الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 113 |  |  |
| | | from | 113 | | |
Abstract
Cirrhosis is caused by hepatic injury that causes necroinflammation and fibrogenesis; histologically, it is defined by diffuse nodular regeneration surrounded by dense fibrotic septa, followed by parenchymal extinction and collapse of liver structures, resulting in a distortion of hepatic vascular architecture. Egypt’s high HCV sero prevalence makes liver cirrhosis more prevalent than predicted.
PH is an essentially certain consequences of cirrhosis, and it is responsible for the syndrome’s major fatal consequences: GOV, severe GIT haemorrhage, ascites, HRS, and HE.
GOV are the most significant portosystemic collaterals due to the fact that their rupture causes VH, the most frequent fatal consequence of cirrhosis. Varices and VH are the most directly related consequences of cirrhosis from PH.
UGIE continues to be the best method for screening, however this test has its own limits. If it were feasible to predict EV using noninvasive methods, testing would be limited to the group who appeared to be at the greatest risk, and endoscopies would be performed less often. This screening test should be easy, rapid, repeatable, and cheap.
All cirrhotic patients should be screened for varices at the time of diagnosis, with follow-up every 2 to 3 years for patients without varices (and every 1 to 2 years for patients with small varices to assess for varices enlargement and the need for prophylactic treatment. Current criteria create a tremendous load and expense on endoscopy facilities and require patients to repeat uncomfortable procedures, even though 50% may not have EV 10 years after the original diagnosis.
Due to the expense and invasiveness of endoscopic screening, there is an urge to create noninvasive indicators for EV that would reduce the number of OGDs conducted.
There are a wide variety of cells in the body that secrete CHI3L1, also known as YKL-40 and found in macrophages, chondrocytes and HSCs. Humans have a gene called CHI3L1 that causes the protein to be produced.