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Pathogenesis of portal hypertensive gastropathy: translating basic research into clinical practice

Abstract

Portal hypertensive gastropathy (PHG) is often seen in patients with portal hypertension, and can lead to transfusion-dependent anemia as well as acute, life-threatening bleeding episodes. This Review focuses on the mechanisms that underlie the pathogenesis of PHG that provide reasonable grounds for the treatment of this condition, and ultimately enable translation of basic research into clinical practice. Increased portal pressure associated with cirrhosis and liver dysfunction is critical for the development of clinically significant PHG, and leads to impaired gastric mucosal defense mechanisms that render the stomach susceptible to mucosal injury. The use of pharmacological agents such as β-blockers reduces the frequency of bleeding episodes in PHG. As a last resort, surgical decompression of the portal system, transjugular intrahepatic stent placement and liver transplantation can resolve this condition. Elimination of known risk factors for gastric injury such as alcohol, aspirin and traditional NSAIDs is critical. The role of Helicobacter pylori colonization of the gastric mucosa in PHG is not clear. Careful and critical interpretation of human and experimental data can be helpful to establish a rationale for the medical management of this important condition.

Key Points

  • Portal hypertensive gastropathy (PHG) is frequently observed in patients with portal hypertension, with and without cirrhosis

  • Patients with cirrhosis and portal hypertension often present with transfusion-dependent anemia, and the stomach of these patients is highly susceptible to injury induced by irritants such as ethanol, aspirin and traditional NSAIDs

  • Portal hypertension is necessary but perhaps not sufficient for the development of clinically significant PHG

  • Liver dysfunction has a role in the increased susceptibility of the portal hypertensive gastric mucosa to injury and spontaneous bleeding

  • Several pharmacological agents can be employed to treat bleeding episodes associated with PHG—β-blockers seem to be beneficial in preventing recurrent bleeding and acid-secretion blockers are important in the treatment of documented gastric damage

  • Endoscopic treatment of esophagogastric varices might enhance PHG

  • Resolution of PHG can be achieved with surgical decompression of the portal system, placement of a transjugular intrahepatic shunt, or liver transplantation

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Figure 1: Endoscopic images of portal hypertensive gastropathy that show the four main findings of this condition.

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Correspondence to Jose GP Ferraz.

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Perini, R., Camara, P. & Ferraz, J. Pathogenesis of portal hypertensive gastropathy: translating basic research into clinical practice. Nat Rev Gastroenterol Hepatol 6, 150–158 (2009). https://doi.org/10.1038/ncpgasthep1356

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