الفهرس 
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Abstract
Portal hypertension is a clinical syndrome defined as the pathologic increase of portal pressure gradient above its upper normal limit of 5 mmHg. Its importance lies in the frequency and severity of its complications, namely porto-systemic collaterals, variceal hemorrhage, ascites, hepato-renal syndrome, porto-systemic encephalopathy and hepato-pulmonary syndrome. The appearance of these complications defines progression of liver disease to the decompensated stage.
The most common world wide cause of portal hypertension is liver cirrhosis due to alcoholic hepatitis in western countries or post HCV infection in developing countries like Egypt. While Bilharzial periportal fibrosis represents another important cause in Egypt. Other relatively frequent extrahepatic causes of PHT include PVT and BCS.
PHT is initiated by increased resistance to portal blood flow which may be at the prehepatic, intrahepatic or at the post-hepatic levels. The intrahepatic resistance to portal blood flow is increased due to both mechanical component (fibrosis and vascular occlusion) and dynamic component caused by endothelial dysfunction that leads to an increase in the intrahepatic vascular tone.
Endothelial dysfunction outside the liver microcirculation also shares in the pathogenesis of PHT by increasing portal blood flow through splanchnic vasodilatation and hyperdynamic circulation. Angiogenesis can also increase portal blood flow and shares in the formation of porto-systemic collateral vessels, the resistance of which can further adds to the resistance of the portal venous system.
The most reliable method for diagnosing PHT is the measurement of the portal pressure and the HVPG. Unfortunately, their measurement is invasive and cannot be routinely done in every patient. Therefore, alternative minimally invasive or noninvasive methods such as EGD, endoscopic ultrasound, video capsule endoscopy, multidetector CT esophagography and others should be used in the process of diagnosing and monitoring patients with PHT. All these diagnostic modalities have its own advantage and disadvantage in diagnosing and monitoring PHT as well as its complications. Many blood markers of liver fibrosis were also pro-posed as noninvasive means for diagnosing PHT like those reflecting the degree of HSC activation as an indirect method of detecting PHT.
Current treatment modalities for portal hypertension rely on decreasing portal blood inflow to reduce the elevated portal pressure. These modalities aim at treating complications of PHT rather than treating PHT itself. Varices are the most common and most feared of these complications. Patients with varices that had never bled before are currently treated with either non selective beta blockers, like propranolol, or endoscopic variceal ligation according to the clinical situation. While endoscopic intervention, either by EVL or EIS plus using pharmacotherapy after patient stabilization are considered the first line treatment in patients presented by an acute variceal bleeding episode. Second line treatment of these patients include balloon tamponade, TIPS and surgery. Non selective beta blockers and endoscopic treatment, either by EVL or EIS, are used for secondary prophylaxis against variceal bleeding. These management strategies still have an unsatisfactory outcome and this would raise our attention to find out more effective therapies for better treatment of PHT not its complication that will be prevented accordingly.
Future (prospective) therapy of PHT is expected to be more causal in nature and so it would be able to stop the progression of the original liver disease or any pathologic state that can maintain or aggravate PHT. Endothelial dysfunction is an important target for the future therapy. Also, targeting the mechanical component of the increased IHVR by using antifibrotic therapies seems to be promising. The strategy of such future therapy necessitates removal of any injurious stimuli and treatment of the original liver disease like treatment of viral hepatitis C and B. It also involve suppression hepatic inflammation, downregulation of HSC activation, enhancing fibrinolysis and using various cytokine targeted therapies like these targeting angiogenesis or fibrogenesis or both, like these antagonizing VEGF and PDGF like Sorafinib.
Prospective therapy seems promising, offering portal hypertensive patients more hope about the possibility of better treatment in condition of early treatment. A prerequisite that demonstrates the importance of developing new effective diagnostic tools for activating contentious surveillance and early detection of liver diseases, specially the chronic of them, and PHT in high risk group patients. Also, to develop these prospective therapy to be available for treating patients rather than being an experimental findings.