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 beta-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.

Portal Hypertensive Gastropathy: Correlation with Portal Hypertension and Prognosis in Cirrhosis

“…Portal hypertensive gastropathy (PHG) is a common finding in patients with liver cirrhosis and portal hypertension, and PHG is one of the causes of gastrointestinal blood loss [1][2][3]. The diagnosis is made endoscopically, and the degree of PHG is classified as mild or severe [4].…”

“…The diagnosis is made endoscopically, and the degree of PHG is classified as mild or severe [4]. PHG can progress from mild to severe and vice versa over time, and it has been suggested that various factors, including luminal irritants such as alcohol, bile salts, and non-steroidal anti-inflammatory drugs (NSAIDs), are associated with the progression of PHG [1,2]. However, increased portal pressure and liver dysfunction are critical for the development of PHG in cirrhosis [1][2][3].…”

“…PHG can progress from mild to severe and vice versa over time, and it has been suggested that various factors, including luminal irritants such as alcohol, bile salts, and non-steroidal anti-inflammatory drugs (NSAIDs), are associated with the progression of PHG [1,2]. However, increased portal pressure and liver dysfunction are critical for the development of PHG in cirrhosis [1][2][3]. Very few studies have directly evaluated the relationship between the degree of portal hypertension and PHG, and the results are controversial [4][5][6][7][8].…”

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

“…Hashizume et al [116] reported that cirrhotic patients have dilated small gastric blood vessels, including arterioles, precapillaries, capillaries, submucosal veins, and subserosal veins, with decreased arteriovenous resistance and straightening of arterioles. Percutaneous transhepatic variceal embolization [85] This hyperdynamic circulation impairs gastric mucosal defense mechanisms, causes release of proinflammatory mediators, and inhibits growth factors which render gastric mucosa more susceptible to injury [67,117] and impair mucosal healing [113,114,118,119] . This vulnerable mucosa becomes predisposed to bleeding [117,120] .…”

“…Percutaneous transhepatic variceal embolization [85] This hyperdynamic circulation impairs gastric mucosal defense mechanisms, causes release of proinflammatory mediators, and inhibits growth factors which render gastric mucosa more susceptible to injury [67,117] and impair mucosal healing [113,114,118,119] . This vulnerable mucosa becomes predisposed to bleeding [117,120] . Decreased gastric mucosal perfusion may explain the increased rate of erosions, ulcers, and bleeding in PHG [118] .…”