Gastric permeability to sucrose is increased in portal hypertensive gastropathy

Giofré, M.R.; Meduri, G. Umberto; Pallio, Socrate; Calandra, S.; Magnano, Antonio; Niceforo, D.; Cinquegrani, Michael; Leo, Vincenza Di; Mazzon, Emanuela; Sturniolo, Giacomo Carlo; Longo, G; Fries, Walter

doi:10.1097/00042737-200012050-00009

Cited by 23 publications

(14 citation statements)

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“…Two studies have documented normal passive permeability in cirrhotics [22,23]. In contrast, Taylor et al reported increased small bowel permeability in children with cirrhotic and noncirrhotic portal hypertension and Giofre et al found that patients with portal hypertensive gastropathy had increased gastric permeability [25]. Our data are in agreement with the recent report of De Leo and colleagues [26], who also found increased intestinal permeability in patients with PBC.…”

Section: Discussionsupporting

confidence: 91%

Abnormal Intestinal Permeability in Primary Biliary Cirrhosis

2006

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Antimitochondrial antibodies (AMAs) found in patients with primary biliary cirrhosis (PBC) cross-react with bacterial proteins and hence molecular mimicry has been proposed as a mechanism for AMA development. Alterations in gastrointestinal permeability would provide a potential route for increased exposure of gut flora to the immune system. In this study we aimed to compare the measured gastrointestinal permeability in patients with PBC to that in patients with liver disease (hepatitis C) and healthy control populations. Subjects drank a mixture of sucrose, lactulose, and mannitol dissolved in water. Eight-hour urinary excretion of the sugars was measured to assess intestinal permeability. Antiendomysial antibody testing was performed to exclude subclinical celiac disease. Eighty-six patients with PBC were evaluated and compared to 69 hepatitis C patients and 155 healthy controls. The mean urinary excretion of sucrose in the PBC patients (133.89 +/- 72.56 mg) was significantly higher than that in hepatitis C patients (101.07+/-63.35) or healthy controls (89.46+/-41.76) (P=0.0001), suggesting abnormal gastric or proximal small intestinal permeability. Sucrose excretion was not increased among patients with hepatitis C compared to healthy controls. The ratio of lactulose:mannitol excretion, reflecting small bowel permeability, was also elevated in the PBC group (0.017+/-0.012) compared to healthy controls (0.012+/-0.007) (P=0.0001) but was equal to that found among patients with hepatitis C (0.016+/-0.011) (P=NS). We conclude that the permeability of both the stomach and the small bowel is increased in patients with PBC, however, it is unclear if it is a cause, consequence, or manifestation of the disease.

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Section: Discussionsupporting

confidence: 91%

Abnormal Intestinal Permeability in Primary Biliary Cirrhosis

2006

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“…Helicobacter pylori: Numerous studies demonstrated that Helicobacter pylori (H. pylori) infection is not associated with PHG [7,9,25,79,109,110,154,[168][169][170][171][172] . Indeed, several studies reported that patients with PHG less frequently have H. pylori infection than controls.…”

Section: Other Cytokines and Growth Factorsmentioning

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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“…In a large cohort of cirrhotic patients, the presence of portal hypertension and ascites was an independent determinant of intestinal permeability in addition to age, alcohol intake, and diabetes ( 68 ). Gastric permeability was increased in patients with portal hypertensive gastropathy ( 71 ). Insertion of TIPSS and treatment with propanolol were found to improve intestinal permeability ( 72,73 ).…”

Section: Mechanisms Of Bacterial Translocationmentioning

confidence: 99%

Clinical and Pathophysiological Consequences of Alterations in the Microbiome in Cirrhosis

Macnaughtan

Jalan

2015

American Journal of Gastroenterology

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Cirrhosis is a major cause of mortality worldwide. Exponential rises in prevalence have been observed secondary to increases in obesity and alcohol consumption. Multiple lines of evidence implicate gut-derived bacteria and bacterial ligands as a central driver of pathogenesis. Recent developments in culture-independent techniques have facilitated a more accurate description of microbiome composition in cirrhosis and led to the description of measures of dysbiosis shown to be associated with disease. More importantly, metagenomic studies are adding to an understanding of the functional contribution of the microbiota and may prove to be a more clinically relevant biomarker than phylogenetic studies. Much like other dysbiotic states such as inflammatory bowel disease, the microbiota in cirrhosis is characterized by a low microbial and genetic diversity. Therapeutic strategies to diminish this process are currently limited to selective intestinal decontamination with antibiotics. This review summarizes the available data and develops a framework for the use of current and future treatment strategies to diminish the consequences of dysbiosis in cirrhosis. Interventional strategies to bind bacterial products in the gut lumen and blood, and modulate the magnitude of host sensing mechanisms remain an unmet clinical need. A greater understanding of the host-microbiota interaction in cirrhosis is of key importance to inform future interventional strategies to diminish the currently escalating burden of the disease.

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Gastric permeability to sucrose is increased in portal hypertensive gastropathy

Cited by 23 publications

References 0 publications

Abnormal Intestinal Permeability in Primary Biliary Cirrhosis

Abnormal Intestinal Permeability in Primary Biliary Cirrhosis

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

Clinical and Pathophysiological Consequences of Alterations in the Microbiome in Cirrhosis

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