Portal-hypertensive gastropathy develops less in patients with cirrhosis and fundal varices

Iwao, Tadashi; Toyonaga, Atsushi; Oho, Kazuhiko; Sakai, Teruhiro; Tayama, Chizuru; Masumoto, Hideo; Sato, Masahiro; Nakahara, K; Tanikawa, Kyuichi

doi:10.1016/s0168-8278(97)80457-6

Cited by 43 publications

(50 citation statements)

References 28 publications

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“…Iwao et al [31] in an endoscopic study of 47 patients with histologically-proven cirrhosis reported no significant differences in etiology of cirrhosis between patients without PHG vs patients with mild or severe PHG. Iwao et al [31] reported no association between etiology of cirrhosis and PHG severity. The etiologies of cirrhosis in this study included 7 from alcoholism vs 8 from chronic hepatitis in patients without PHG, 5 from alcoholism vs 10 from chronic hepatitis in patients with mild PHG, and 8 from alcoholism vs 9 from chronic hepatitis in patients with severe PHG (NS).…”

Section: Cirrhotic Vs Non-cirrhotic Portal Hypertensionmentioning

confidence: 94%

“…Gupta et al [30] in a study of 230 patients with cirrhosis and esophageal varices found no significant difference in the rate of PHG between patients with cirrhosis from alcohol [32 of 52 patients (62%)] vs cirrhosis from other causes [110 of 178 patients (62%), P = NS]. Iwao et al [31] in an endoscopic study of 47 patients with histologically-proven cirrhosis reported no significant differences in etiology of cirrhosis between patients without PHG vs patients with mild or severe PHG. Iwao et al [31] reported no association between etiology of cirrhosis and PHG severity.…”

Section: Cirrhotic Vs Non-cirrhotic Portal Hypertensionmentioning

confidence: 97%

“…Contrariwise, a decided minority of studies showed no significant association between severity of portal hypertension and rate of PHG [8,9,16,26,28,30,31,47,54,67] .…”

Section: (50%) Not Reported Not Reportedmentioning

confidence: 98%

“…Likewise, Gupta et al [30] reported a significantly higher prevalence of PHG in patients with esophageal and gastric varices [74 of 107 patients (69%)] compared to solely esophageal varices [68 of 123 patients (55%), P < 0.05]. Iwao et al [31] reported a significantly higher incidence of PHG in cirrhotic patients with esophageal varices as compared to fundal gastric varices. Merkel et al [36] reported that patients with severe PHG localized to the gastric body or fundus had significantly higher HVPG than patients with severe PHG localized to the gastric antrum.…”

Section: Location Of Varicesmentioning

confidence: 99%

“…Primignani et al [34] confirmed the correlation of PHG with severity of portal hypertension, by correlating PHG with presence and size of esophageal varices. Sacchetti et al [24] Cirrhosis 142 38 (27%) 28 (20%) 10 (7%) D'Amico et al [25] Cirrhosis 212 130 (61%) 110 (52%) 20 (9%) Calès et al [26] Cirrhosis 100 98 (98%) 57 (57%) 41 (41%) Rabinovitz et al [27] Cirrhosis 510 (43%) Not reported Not reported Iwao et al [28] Cirrhosis 47 32 (68%) 15 (32%) 17 (36%) Taranto et al [29] Cirrhosis 394 317 (80.5%) Not reported Not reported Gupta et al [30] Cirrhosis 230 (61%) (52%) (9%) Iwao et al [31] Cirrhosis 476 254 (53%) 208 (43%) 46 (9%) Carpinelli et al [32] Cirrhosis 566 362 (64%) 192 (34%) 170 (30%) Zaman et al [33] Cirrhosis 120 74 (62%) 47 (39%) 27 (23%) Primignani et al [34] Cirrhosis 373 299 (80%) 127 (34%) 172 (46%) Chaves et al [35] Cirrhosis vs schistosomiasis 43 18 (81%) vs 7 (33%) Not reported Not reported Merkel et al [36] Cirrhosis 62 49 (79%) 29 (46%) 20 (32%) Merli et al [37] Cirrhosis, with mild portal hypertension 222 48 (21%) 43 (19%) 5 (2%) Ito et al [38] Cirrhosis 47 13 (27%) 10 (21%) 3 (6%) De Palma et al [39] Cirrhosis 37 23 (62%) Not reported Not reported Menchén et al [40] Cirrhosis 549 353 (64%) 275 (50%) 77 (14%) Yüksel et al [41] Cirrhosis 114 total 76 (66%) 38 (33%) 38 (33%) Fontana et al [42] Cirrhosis or bridging fibrosis from hepatitis C 1016 374 (37%) 345 (34%) 29 (3%) Bresci et al [43] Cirrhosis 85 36 (42%) Not reported Not reported Akatsu et al [44] End stage liver disease 29 19 (65.5%) 18 (62.1%) 1 (3.4%) Zardi et al [45] Cirrhosis 266 84 (31%) Not reported Not reported Barakat et al [46] Cirrhosis with portal hypertensive duodenopathy 105 105 (100%) 17 (16.2%) 88 (83.8%) Bellis et al [47] Cirrhosis 59 44 (76%) 16 (27%) 28 (47%) Gravante et al [48] Liver transplant candidates with cirrhosis 80 41 (51.2%) Not reported Not reported Canlas et al [49] [58] Cirrhosis 611 448 (73.3%) 37.3% 36% Abbasi et al [59] Cirrhosis 102 87 (85%) Not reported Not reported Ahmed et al …”

Section: (50%) Not Reported Not Reportedmentioning

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: Cirrhotic Vs Non-cirrhotic Portal Hypertensionmentioning

confidence: 94%

Section: Cirrhotic Vs Non-cirrhotic Portal Hypertensionmentioning

confidence: 97%

“…Contrariwise, a decided minority of studies showed no significant association between severity of portal hypertension and rate of PHG [8,9,16,26,28,30,31,47,54,67] .…”

Section: (50%) Not Reported Not Reportedmentioning

confidence: 98%