Esophageal Varices, a Common Manifestation of Portal Hypertension
Chronic liver injury can lead to a sequence of changes that terminates with fatal bleeding from esophageal blood vessels. In most forms of chronic liver injury, stellate cells are transformed into collagen-secreting myofi-broblasts. These cells deposit collagen into the sinusoids, interfering with the exchange of compounds between the blood and hepatocytes and increasing resistance to portal venous flow. The resistance appears to be further increased when stellate cells contract. The increased resistance results in increased hepatic portal pressure and decreased liver blood flow. This disorder is seen in approximately 80% of patients with cirrhosis. In a compensatory effort, new channels are formed or dormant venous tributaries are expanded, resulting in the formation of varicose (unnaturally swollen) veins in the abdomen. Although varicose veins develop in many areas, portal pressure increases are least opposed in the esophagus because of the limited connective tissue support at the base of the esophagus. This structural condition, along with the negative intrathoracic pressure, favors the formation and rupture of esophageal varices. Approximately 30% of patients who develop an esophageal variceal hemorrhage die during the episode of bleeding, making it one of the most lethal medical illnesses.
Currently there are no well-recognized treatments to reverse cirrhosis, but numerous strategies are employed to reduce portal hypertension and bleeding. Chief among these is the use of nonselective beta blockers, which enhance splanchnic arteriolar vasoconstriction and thereby reduce portal venous pressure. Bleeding esophageal varices are frequently treated by endoscopic ligation of the varices. Shunts can be placed radiologically or surgically between the portal venous system and the systemic venous to reduce the portal pressure.
In contrast, cell death that results from necroinflammatory processes is characterized by a loss of cell membrane integrity and the activation of inflammatory reactions. Liver cell suicide is mediated by proapoptotic signals, such as tumor necrosis factor (TNF).
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