Gastric endoscopic features in portal hypertension: final report of a consensus conference, Milan, Italy, september 19, 1992

Spina, G. P.; Arcidiacono, R; Bosch, Jaime; Pagliaro, Luigi; Burroughs, Andrew K.; Santambrogio, Roberto; Rossi, Alfredo

doi:10.1016/s0168-8278(05)80329-0

Cited by 122 publications

(73 citation statements)

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“…In the HALT-C trial, 374 (37%) of 1011 patients with biopsy-proven cirrhosis or bridging fibrosis from hepatitis C had PHG [69] . This wide variability likely reflects variability in classification criteria, interpretation of endoscopic lesions, study populations, and natural history of PHG [10,70,71] . PHG is usually mild as reported by McCormack et al [3] or in the NIEC study [32,70] .…”

Section: Epidemiologymentioning

confidence: 99%

“…This wide variability likely reflects variability in classification criteria, interpretation of endoscopic lesions, study populations, and natural history of PHG [10,70,71] . PHG is usually mild as reported by McCormack et al [3] or in the NIEC study [32,70] . The prevalence of mild PHG in patients with portal hypertension ranges from 29%-57%, and of severe PHG ranges from 9%-46% [71] .…”

Section: Epidemiologymentioning

confidence: 99%

“…Contrariwise, a minority of studies found no correlation between liver disease severity, as determined by Child-Pugh stage, and presence or severity of PHG [34,36,40,47,54,62,70,79] . For example, Primignani et al [34] reported the prevalence of severe PHG was lowest in ChildPugh stage C. In the NIEC study, patients with ChildPugh stage B had a higher prevalence of PHG than patients with stages A or C. Zardi et al [67] reported no significant differences in Child-Pugh stage or in MELD score among cirrhotic patients with vs without PHG.…”

Section: Liver Disease Durationmentioning

confidence: 99%

“…The red lesions vary in size and in color depending on PHG severity. The lesions range from pink speckled lesions within a mosaic or snakeskin pattern in mild cases, to localized small areas of intense erythema, resembling a scarlatina rash, in severe cases [70,71,112,139] . These findings occur predominantly in the gastric body and fundus, and rarely in the antrum [71,72,139] .…”

Section: Diagnosismentioning

confidence: 99%

“…PHG can be simply categorized as mild with a mosaic-like pattern without red spots, or as severe, with superimposed red lesions present [78,96] . Multiple formal endoscopic classifications exist (Table 8 [3,7,8,70,[180][181][182][183] ), with no consensus as to which classification is the best [5,[182][183][184] . The following classifications are commonly used: Classifications by McCormack et al [3] , Tanoue et al [180] , the New Italian Endoscopic Classification (NIEC) [70] , and the Baveno scoring system [181] .…”

Section: Diagnosismentioning

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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