Prevalence of gastric ulcer in cirrhotic patients and its relation to portal hypertension

Chen, Ling-Sheng; H, Lin; Hwang, Shinn‐Jang; Lee, Fa-Yauh; Hou, Ming‐Chih; Lee, Shou‐Dong

doi:10.1111/j.1440-1746.1996.tb00011.x

Cited by 72 publications

(52 citation statements)

References 46 publications

(6 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Compared to healthy controls, patients with liver cirrhosis have been reported to have higher increased plasma gastrin [39] and higher prevalence of peptic ulcers [40,41]. In an endoscopic study, the annual incidence rate of peptic ulcer observed in 140 patients undergoing endoscopic follow-up was 4.3% [42].…”

Section: Structural Changes Of the Gi Tractmentioning

confidence: 99%

“…Compared to healthy controls, patients with liver cirrhosis have been reported to have increased plasma gastrin [39] and higher prevalence of peptic ulcers [40,41]. This may partly explain the consumption of acid secretion inhibitors, but it is possible that there is a certain degree of overuse in these patients in view of the fact that peptic ulcers are asymptomatic in as many as 70% of cases [42].…”

Section: Gastrointestinal Symptoms (I)mentioning

confidence: 99%

See 1 more Smart Citation

Intestinal permeability in cirrhotic patients with and without ascites

Kalaitzakis

Johansson

Bjarnason³

et al. 2006

Scandinavian Journal of Gastroenterology

View full text Add to dashboard Cite

Malnutrition is a common finding in patients with liver cirrhosis. Malnutrition has been shown to be associated with increased morbidity and mortality. Its pathogenesis remains unclear but both poor dietary intake and increased energy expenditure have been reported.Spontaneous bacterial peritonitis is an important clinical problem in cirrhotics. It may occur as a consequence of repeated access of bacteria from the intestinal lumen (translocation) to the mesenteric lymph nodes. One of the mechanisms proposed to explain bacterial translocation in cirrhosis includes increased intestinal permeability.The aims of the present study were to evaluate GI symptoms in cirrhotic patients and their possible relation to nutritional status, to assess whether gastric sensorimotor dysfunction or metabolic disturbances are associated with reduced food intake, and to investigate the role of ascites in intestinal permeability in patients with liver cirrhosis.Gastrointestinal symptoms and health-related quality of life (HRQOL) were assessed with the aid of two questionnaires. Gastric sensorimotor function was measured by means of an electronic barostat. Food intake, as assessed with a food diary, was related to fasting and postprandial glucose, insulin, leptin, and ghrelin concentrations. Intestinal permeability was evaluated by a 51 Cr-EDTA permeability test. Cirrhotics were found to have increased severity of GI symptoms compared with reference values from the general population. A relationship between GI symptoms and compromised HRQOL as well as weight loss was observed.Proximal stomach relaxation to a meal was increased in patients with liver cirrhosis as compared with healthy controls but the relation between gastric accommodation and energy intake was found to be disturbed in these patients. Gastric sensitivity to distension was shown to be related to GI symptom severity and to liver cirrhosis severity scores.Patients with liver cirrhosis exhibited higher postprandial insulin and glucose concentrations compared to controls. Cirrhotics had higher fasting leptin that fell significantly postmeal and they showed an attenuated increase of ghrelin before the next expected meal. Altered glucose and hormonal levels in patients with cirrhosis were associated with poor food intake.Only a few patients with cirrhosis had increased intestinal permeability, as assessed by a 51 Cr-EDTA test, which was not influenced to a major extent by ascites. Conclusions: In patients with liver cirrhosis GI symptom severity is high and it is associated with impaired HRQOL and weight loss. Gastric accommodation is not involved in the poor food intake observed in cirrhotics and gastric sensitivity seems to be a relevant factor for GI symptom generation in these patients. Altered postprandial glucose, leptin, and ghrelin levels are correlated to reduced energy intake in this patient group. Increased intestinal permeability is probably of limited importance in the pathophysiology of bacterial infections in patients with liver cirrhosis and ascites.

show abstract

Section: Structural Changes Of the Gi Tractmentioning

confidence: 99%

Section: Gastrointestinal Symptoms (I)mentioning

confidence: 99%

Intestinal permeability in cirrhotic patients with and without ascites

Kalaitzakis

Johansson

Bjarnason³

et al. 2006

Scandinavian Journal of Gastroenterology

View full text Add to dashboard Cite

show abstract

“…Portal hypertensive gastro- and duodenopathy is defined by enlarged mucosal and submucosal vessels with little or no inflammatory infiltrate or epithelial erosion [50]. This is associated with increased susceptibility to injury from noxious factors reflected in an increased prevalence of peptic ulcer in cirrhotic patients [51]. Factors mediating mucosal damage and impairing the mucosal healing response to injury in advanced cirrhosis may include a reduction of potential differences in gastric mucosa [52], impairment of bicarbonate secretion [53,54], impairment of gastric oxygenation [55], suppression of endogenous prostaglandin production and excessive NO production [56,57,58] as well as increased oxidative stress due to reduced levels of glutathione peroxidase, superoxide dismutase and catalase [59].…”

Section: Intestinal Hyperpermeabilitymentioning

confidence: 99%

Changes of Intestinal Functions in Liver Cirrhosis

2016

View full text Add to dashboard Cite

Background: Understanding of the gut-liver axis is important for the up-to-date management of liver cirrhosis, and changes of intestinal functions form the core of this interesting research field. Summary: Most investigators noted small intestinal dysmotility in their patients with liver cirrhosis. Marked changes in the contraction pattern were observed in early manometric studies. The orocecal transit time, particularly small intestinal transit, has generally been reported to be prolonged, which has been demonstrated in multiple investigations to be related to the severity of the liver disease (e.g., Child-Pugh class), the presence of small intestinal bacterial overgrowth (SIBO) and hepatic encephalopathy (HE) as well as a history of spontaneous bacterial peritonitis. Bacteriologically proven SIBO in proximal jejunal aspiration has been reported to be present in up to 59% of cirrhotic patients and is associated with systemic endotoxemia. Clinical and experimental studies suggest that delayed small bowel transit in liver cirrhosis may lead to SIBO, which could contribute to the symptoms of abdominal pain and diarrhea. In addition to autonomic neuropathy, metabolic derangements and diabetic state, SIBO itself may delay intestinal transit in cirrhotic patients. Several studies, both from the West and the East, have shown that the gut microbiota is altered in cirrhotic patients and particularly those with HE. Further, a quantitative change in Bacteroides/Firmicutes ratio, with a prevalence of potentially pathogenic bacteria (e.g., Enterobacteriaceae) and reduction in specific commensals (e.g., Lachnospiraceae), has been described. Structural and functional changes in the intestinal mucosa that contribute to increases in intestinal permeability for bacteria and their products have been observed in patients with liver cirrhosis, which is considered as an important pathogenetic factor for several complications. The mechanism of intestinal barrier dysfunction in cirrhosis is multifactorial, including alcohol, portal hypertension (vascular congestion and dysregulation), endotoxemia, SIBO, local inflammation and, most likely, immunological factors and medications. Key Messages: This review summarizes major achievements regarding intestinal dysfunction in cirrhosis for future gastroenterology research. The question of whether this intestinal barrier dysfunction is accompanied and/or at least partly caused by structural and functional changes in the epithelial tight junction proteins is as yet unsolved. Development of new strategies to modulate gut-liver interaction is urgently needed.

show abstract

“…The prevalence of H. pylori in patients with cirrhosis and PUD is generally less than 60% [60,[62][63][64][65] , suggesting that the pathogenesis of ulcer disease in a substantial proportion of cirrhotic patients may not be related to H. pylori infection [66][67][68][69] . Host environments are crucial to H. pylori colonization [7,70] .…”

Section: H Pylori Eradication and Recurrent Peptic Ulcers In Patientmentioning

confidence: 99%