Do Alterations in the Rate of Gastric Emptyingafter Injection Sclerotherapy for OesophagealVarices Play any Role in the Developmentof Portal Hypertensive Gastropathy?

Balan, K. K.; Grime, J. S.; Sutton, R.; Critchley, M.; Jenkins, S. A.

doi:10.1155/1999/27037

Cited by 13 publications

(5 citation statements)

References 12 publications

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“…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%

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: 99%

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

Gjeorgjievski¹

2016

WJH

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“…A recent study suggested that autonomic neuropathy (AN) contributes to the formation of gallstones in patients with advanced cirrhosis (4). Acceleration, delay, or no significant change in gastric emptying in patients with cirrhosis was reported by a number of studies (5)(6)(7)(8)(9). AD seems to affect biliary motility directly through the neural pathway and/or indirectly through the probable effect of alteration in gastric emptying on CCK secretion.…”

Section: Introductionmentioning

confidence: 97%

Autonomic neuropathy and gallbladder motility in patients with liver cirrhosis

Kul¹,

Serin²,

Yakar³

et al. 2015

Turk J Gastroenterol

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Background/Aims: Impaired gallbladder motility has been suggested as a contributor to increased incidence of gallstones in patients with liver cirrhosis. The purpose of this study was to determine gallbladder function and its relation with autonomic neuropathy in liver cirrhosis. Materials and Methods: Gallbladder function was measured using ultrasonography in 48 patients with liver cirrhosis and in 31 controls. Autonomic neuropathy tests were applied in patients with liver cirrhosis. Patients with liver cirrhosis were analyzed in subgroups according to the severity of disease using the Child-Pugh classification. Results: Fasting gallbladder volume was 16.2 mL (range: 2.1 mL-71.9 mL) in patients and 17.6 mL (range: 4.9 mL-76.6 mL) in controls. There were no differences in fasting gallbladder volume among the study groups (p>0.05). Gallbladder ejection fraction was significantly higher in patients compared with controls (84% vs. 65%) (p<0.001). No correlation was found between gallbladder ejection fraction and autonomic neuropathy (p>0.05). Conclusion: Our results indicate that liver cirrhosis does not impair gallbladder emptying, and that there is no association between gallbladder motility and autonomic neuropathy. Further investigations are required to explain increased gallbladder motility in liver cirrhosis.

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“…Balan et al . [ 11 ] observed that the gastric emptying was disturbed in patients with portal hypertension and received sclerotherapy, which may contribute to portal hypertensive gastropathy. Gastroparesis in patients with liver cirrhosis may be due to autonomic dysfunction, which correlated positively with delayed gastric emptying.…”

Section: Discussionmentioning

confidence: 99%

“…[ 5 25 26 ] A delay in gastric emptying in patients with portal hypertension can aggravate or lead to the development of portal hypertensive gastropathy due to the deleterious effects of endogenous substances, such as acid and pepsin. [ 11 ]…”

Section: Discussionmentioning

confidence: 99%

Measuring of gastric emptying in Egyptian pediatric patients with portal hypertension by using real-time ultrasound

Fahmy

Osman

Mahmoud

et al. 2012

Saudi J Gastroenterol

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Background/Aim:Among the various methods for evaluating gastric emptying, the real-time ultrasound is safe, does not require intubation, or rely on either radiologic or radionuclide technique. The aim of our work was to measure the gastric emptying in pediatric patients with portal hypertension by using the real-time ultrasound.Patients and Methods:Forty patients with portal hypertension with mean age 7 ± 2.8 years and 20 healthy children as a control group underwent gastric emptying study by using real-time ultrasound. The cross-sectional area of the gastric antrum was measured in the fasting state and then each subject was allowed to drink tap water then calculated by using formula area (π longitudinal × anteroposterior diameter/4). The intragastric volume was assumed to be directly proportional to the cross-sectional area of the antrum.Results:The mean gastric emptying half-time volume was significantly delayed in portal hypertension patients (40 ± 6.8 min) compared with the control subjects (27.1 ± 3.6) min (P<0.05). Patients with extrahepatic portal vein obstruction had significant delayed gastric emptying in comparison to patients with portal hypertension due to other etiologies (36.14 ± 4.9 vs 44.41 ± 6.04 min; P<0.01).Conclusion:Ultrasound is a noninvasive and a reliable method for measuring gastric emptying in pediatric patients. Gastric emptying was significantly delayed in patients with portal hypertension. Etiology of portal hypertension may influence gastric emptying time in patients with chronic liver disease.

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Do Alterations in the Rate of Gastric Emptyingafter Injection Sclerotherapy for OesophagealVarices Play any Role in the Developmentof Portal Hypertensive Gastropathy?

Cited by 13 publications

References 12 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

Autonomic neuropathy and gallbladder motility in patients with liver cirrhosis

Measuring of gastric emptying in Egyptian pediatric patients with portal hypertension by using real-time ultrasound

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