Review article: the management of portal hypertensive gastropathy and gastric antral vascular ectasia in cirrhosis

Patwardhan, Vilas; Cárdenas, Andrés

doi:10.1111/apt.12824

Cited by 72 publications

(63 citation statements)

References 74 publications

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“…Only 30% of cases [191,192] Sex Mildly more common in males (alcoholic cirrhosis more common in males than females) Much more common in females (80%) [193,194] Age Can occur at any age in patients with portal hypertension or cirrhosis [72,195] Appearance at endoscopy…”

Section: Strong Associationmentioning

confidence: 99%

“…Tortuous columns of ectatic vessels in "watermelon" or diffuse pattern; erythematous or hemorrhagic [191] Histology Ectatic capillaries, mildly dilated mucosal and submucosal veins; no vascular inflammation, no vascular thrombi…”

Section: Strong Associationmentioning

confidence: 99%

“…Marked dilation of capillaries and venules in gastric mucosa and submucosa with areas of intimal thickening, fibrin thrombi, fibromuscular hyperplasia and spindle cell proliferation [72,191,196,197] Clinical presentation/ complications…”

Section: Strong Associationmentioning

confidence: 99%

“…Current pharmacologic therapies aim to reduce portal pressure to decrease bleeding from PHG [191,214] . β-adrenergic receptor antagonists: Nonselective β-adrenergic receptor antagonists reduce portal pressure and gastric mucosal blood flow, and thereby reduce bleeding from PHG [103,104,132,191,[222][223][224] .…”

Section: Pharmacotherapy For Phgmentioning

confidence: 99%

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

Gjeorgjievski¹

2016

WJH

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AIM:To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy (PHG) based on a systematic literature review. METHODS:Computerized search of the literature was performed via PubMed using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS:PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG. Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt and liver transplantation are highly successful ultimate therapies because they reduce the underlying portal hypertension. SYSTEMA...

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Section: Strong Associationmentioning

confidence: 99%

Section: Strong Associationmentioning

confidence: 99%

Section: Strong Associationmentioning

confidence: 99%

Section: Pharmacotherapy For Phgmentioning

confidence: 99%

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

Gjeorgjievski¹

2016

WJH

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“…While portal hypertensive gastropathy is easily identified by EGD, capsule endoscopy is needed for the diagnosis of portal hypertensive enteropathy. The characteristic lesions on endoscopy include diffuse mucosal edema and erosion, red spots, vascular tortuosity and increasing number of vessel and angiectasia [12][13][14]. Management of bleeding from portal hypertensive gastroenteropathy can be challenging often because of diffuse bleeding sites.…”

Section: Discussionmentioning

confidence: 99%

Abdominal Tuberculosis Leading to Prehepatic Portal Hypertension: A Case Report

Feng¹

2014

J Cytol Histol

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Tuberculosis can affect any organ or tissue in the abdomen such as gastrointestinal tract, peritoneum, lymphatic system and solid organs. Lymphadenopathy is the most common manifestation of abdominal tuberculosis which can be the only sign of the disease, especially in the periportal region or combined with peritoneal or solid organ involvement. There are a number of causes for prehepatic noncirrhotic portal hypertension, but there were a few reports of prehepatic portal hypertension associated with tuberculosis. Here we report a rare case of intra-abdominal tuberculosis as a cause for portal hypertension and recurrent gastrointestinal bleeding. Enlarged lymph nodes at hepatic hilum compressed the portal vein which caused portal hypertension and portal hypertensive gastropathy and enteropathy. The patient was managed by anti-tuberculosis therapy followed by splenectomy, surgical portaazygous devascularization and splenorenal shunt. In the 2-year followup after operation, the patient was free of symptoms and had cavernous portal vein transformation on CT, and disappearance of varices and portal hypertensive gastroenteropathy on EGDs.

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Anemia in Liver Disease

Patel

Kappus

Muir

2017

Management of Anemia

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Review article: the management of portal hypertensive gastropathy and gastric antral vascular ectasia in cirrhosis

Abstract: SUMMARY BackgroundPortal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are important causes of both acute and chronic gastrointestinal bleeding in patients with cirrhosis.

Cited by 72 publications

References 74 publications

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

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

Abdominal Tuberculosis Leading to Prehepatic Portal Hypertension: A Case Report

Anemia in Liver Disease

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