Changes in portal hypertensive gastropathy after endoscopic variceal sclerotherapy or ligation: An endoscopic observation

Hou, Ming‐Chih; H, Lin; Chen, Chen-Hsiang; Kuo, Benjamin Ing-Tiau; Perng, Cherng-Kang; Lee, Fa-Yauh; Lee, Shou‐Dong

doi:10.1016/s0016-5107(95)70070-6

Cited by 45 publications

(11 citation statements)

References 26 publications

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“…For example, Sarin et al [10] reported in a study of 84 patients followed for a mean of 25 ± 14 mo that PHG resolved in 28 (44%) of 64 patients who developed PHG after sclerotherapy, but resolved in only 2 (9%) of 22 patients who had PHG present before sclerotherapy (P < 0.05). Hou et al [73] similarly reported that the increased severity of PHG after variceal obliteration was generally transitory and returned to baseline status. The return to baseline severity of PHG was significantly faster after variceal ligation than after sclerotherapy (P = 0.03), attributed to ligation achieving subtotal variceal obliteration and permitting faster redistribution of blood flow [10] .…”

Section: Esophageal Variceal Eradicationmentioning

confidence: 94%

“…Portal hypertension: Most studies show that the frequency and severity of PHG is strongly correlated with the severity of portal hypertension, as indicated by multiple parameters, including hepatic venous pressure gradient (HVPG) [36,57] , esophageal intravariceal pressure [29] , and presence or size of esophageal varices [34,42,57,62,73] . Merkel et al [36] reported that the severity of PHG was correlated with the severity of portal hypertension as determined by HVPG, but this correlation was significant only for severe PHG (HVPG .…”

Section: Risk Factors For Phgmentioning

confidence: 99%

“…Numerous studies demonstrated that PHG increased in incidence and that preexistent PHG increased in severity after eradication of esophageal varices by either endoscopic variceal ligation (Table 3) [41, 73,[80][81][82] or endoscopic variceal sclerotherapy (Table 4) [8,10,11,25,30,41,73,[81][82][83] in cirrhotic patients with portal hypertension. Both phenomena also occurred after endoscopic variceal eradication in patients with non-cirrhotic portal hypertension, as shown in two studies in pediatric patients with EHPVO.…”

Section: Esophageal Variceal Eradicationmentioning

confidence: 99%

“…Data on which technique of endoscopic variceal eradication leads to quantitatively more de novo PHG is contradictory. Most studies showed no differences in frequency or severity of PHG after variceal ligation vs sclerotherapy [19,34,41,73,92,93] , but some studies showed worse outcomes after variceal ligation [82,93,94] , while some other studies showed worse outcomes after sclerotherapy [95] .…”

Section: Esophageal Variceal Eradicationmentioning

confidence: 99%

“…De novo PHG after variceal obliteration is often transitory and less severe than PHG that predated the variceal obliteration [10,73] . For example, Sarin et al [10] reported in a study of 84 patients followed for a mean of 25 ± 14 mo that PHG resolved in 28 (44%) of 64 patients who developed PHG after sclerotherapy, but resolved in only 2 (9%) of 22 patients who had PHG present before sclerotherapy (P < 0.05).…”

Section: Esophageal Variceal Eradicationmentioning

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: Esophageal Variceal Eradicationmentioning

confidence: 94%