Intestinal permeability in patients with chronic liver diseases: Its relationship with the aetiology and the entity of liver damage

Cariello, Rita; Federico, Alessandro; Sapone, Anna; Tuccillo, Concetta; Scialdone, V.R.; Tiso, Angelo; Miranda, Agnese; Portincasa, Piero; Carbonara, Veronica; Palasciano, Giuseppe; Martorelli, L.; Esposito, Pasquale; Cartenı̀, Maria; Blanco, C. Del Vecchio; Loguercio, C.

doi:10.1016/j.dld.2009.05.001

Cited by 80 publications

(70 citation statements)

References 39 publications

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“…The ratio of the lactulose/mannitol excretion calculated from the percentage of recovery of the two sugars was used to determine an index of intestinal permeability. As described by others before a ratio of lactulose/mannitol \0.030 was considered as normal [25][26][27][28]. This cut-off value was the mean ?2 SD value calculated in a large group of healthy subjects [23].…”

Section: Intestinal Permeabilitymentioning

confidence: 99%

Nutrition, Intestinal Permeability, and Blood Ethanol Levels Are Altered in Patients with Nonalcoholic Fatty Liver Disease (NAFLD)

Küper²,

et al. 2012

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Section: Intestinal Permeabilitymentioning

confidence: 99%

Nutrition, Intestinal Permeability, and Blood Ethanol Levels Are Altered in Patients with Nonalcoholic Fatty Liver Disease (NAFLD)

Küper²,

et al. 2012

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“…It has been suggested that acid-suppressive therapy with proton pump inhibitors (PPIs), which is widely used in patients with cirrhosis, may increase the risk of bacterial infections, since they cause bacterial overgrowth in the small intestine and increase intestinal permeability [87][88][89][90][91][92] . Several studies, including a meta-analysis [93] of four studies involving a total of 772 patients [94][95][96][97][98] , found significant association between PPI and the development of SBP in patients with cirrhosis (odds ratio 2.77, 95%CI: 1.82-4.23).…”

Section: Secondary Prophylaxis In Patients With Prior Sbpmentioning

confidence: 99%

Diagnosis and management of bacterial infections in decompensated cirrhosis

Pleguezuelo

Benítez²,

Jurado³

et al. 2013

WJH

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Bacterial infections are one of the most frequent complications in cirrhosis and result in high mortality rates. Patients with cirrhosis have altered and impaired immunity, which favours bacterial translocation. Episodes of infections are more frequent in patients with decompensated cirrhosis than those with compensated liver disease. The most common and life-threatening infection in cirrhosis is spontaneous bacterial peritonitis followed by urinary tract infections, pneumonia, endocarditis and skin and soft-tissue infections. Patients with decompensated cirrhosis have increased risk of developing sepsis, multiple organ failure and death. Risk factors associated with the development of infections are severe liver failure, variceal bleeding, low ascitic protein level and prior episodes of spontaneous bacterial peritonitis (SBP). The prognosis of these patients is closely related to a prompt and accurate diagnosis. An appropriate treatment decreases the mortality rates. Preventive strategies are the mainstay of the management of these patients. Empirical antibiotics should be started immediately following the diagnosis of SBP and the first-line antibiotic treatment is third-generation cephalosporins. However, the efficacy of currently recommended empirical antibiotic therapy is very low in nosocomial infections including SBP, compared to community-acquired episodes. This may be associated with the emergence of infections caused by Enterococcus faecium and extended-spectrum β-lactamaseproducing Enterobacteriaceae, which are resistant to the first line antimicrobial agents used for treatment. The emergence of resistant bacteria, underlines the need to restrict the use of prophylactic antibiotics to patients with the greatest risk of infections. Nosocomial infections should be treated with wide spectrum antibiotics. Further studies of early diagnosis, prevention and treatment are needed to improve the outcomes in patients with decompensated cirrhosis.

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“…In our murine model, the subthreshold xenobiotic DDC is causal as a fibrogenic activator. The third factor is increased intestinal permeability and inflammation, which can be a primary abnormality altering the intestinal integrity, such as that seen in CF or in colitis, which is the major predisposing factor to PSC in humans (9). Accordingly, in our model, DSS was used to induce colitis and alter intestinal permeability (33).…”

Section: Discussionmentioning

confidence: 99%