Effect of cisapride on intestinal bacterial overgrowth and bacterial translocation in cirrhosis

Pardo, Albert; Bartolı́, Ramón; Lorenzo-Zúñiga, Vicente; Planas, Ramón; Viñado, Belén; Riba, Joan; Cabré, Eduard; Santos, J.; Luque, Teresa; Ausina, V.; Gassull, M. A.

doi:10.1053/he.2000.5746

Cited by 163 publications

(117 citation statements)

References 37 publications

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“…We found evidence that factors other than endotoxin influence circulating levels of TNF-␣ and sTNFRs in patients with cirrhosis. Evidence that Gram-positive microbial stimuli may be implicated is consistent with recent reports of a high prevalence of intestinal bacterial overgrowth with Gram-positive bacteria in cirrhotic patients [24][25][26] and findings implying increased translocation of lipoteichoic acid from the intestine in this group. 27 Consequently, we investigated the possible importance of Gram-positive gut flora by studying systemic TLR expression and TNF-␣ levels along with in vitro production of TNF-␣ in cirrhotic patients before, during, and after oral supplementation with a synbiotic (probiotic and prebiotic) regimen that included bacterial species known to enhance intestinal levels of Gram-positive bacteria.…”

supporting

confidence: 91%

Peripheral blood mononuclear cell expression of toll-like receptors and relation to cytokine levels in cirrhosis

et al. 2003

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Activation of macrophages by endotoxin is assumed responsible for increased circulating tumor necrosis factor ␣ (TNF-␣) and soluble TNF receptor (sTNFR) levels in cirrhosis. Relevant to this is expression of Toll-like receptor (TLR) 4 and TLR2, which is critically involved in production of TNF-␣ in response to endotoxin and Gram-positive microbial stimuli, respectively. The first studies on this in cirrhosis are reported here. In 36 cirrhotic patients and 32 controls, we measured (1) circulating endotoxin, TNF-␣, and sTNFR levels; (2) peripheral blood mononuclear cell (PBMC) expression of TLR4 and TLR2, and (3) in vitro TNF-␣ production by PBMCs stimulated with endotoxin or Staphylococcus aureus enterotoxin B (SEB). PBMC expression of TLR2, circulating TNF-␣ levels, and in vitro TNF-␣ production were reassessed after supplementation with a synbiotic regimen known to increase intestinal levels of Gram-positive bacteria. Endotoxin, TNF-␣, and sTNFR levels were significantly increased in cirrhosis. Endotoxin levels did not correlate significantly with other parameters. PBMC expression of TLR2 but not TLR4 was significantly up-regulated in cirrhosis and correlated significantly with serum TNF-␣ and sTNFR levels. In vitro TNF-␣ production by PBMCs stimulated by SEB was significantly blunted. Supplementation with the synbiotic regimen resulted in significant up-regulation of PBMC expression of TLR2. Serum TNF-␣ levels were further increased and in vitro TNF-␣ production further reduced in most patients. In conclusion, up-regulation of PBMC expression of TLR2 but not TLR4 occurs in cirrhosis, which implies, contrary to previous assumptions, an important stimulatory role for Gram-positive microbial components but not endotoxin. TLR2 likely contributes to increased circulating TNF-␣ and sTNFR levels in cirrhosis.

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confidence: 91%

Peripheral blood mononuclear cell expression of toll-like receptors and relation to cytokine levels in cirrhosis

et al. 2003

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“…Nonantibiotic procedures could also be effective in the prevention of infections in cirrhotic patients. 55 We conclude that prophylaxis with norfloxacin favors the development of infections caused by norfloxacin-resistant E. coli, mainly in patients on continuous long-term prophylaxis. This finding speaks against the widespread use of prophylaxis, that should be restricted to highly selected groups at high risk of infection closely monitored for the development of bacterial resistance.…”

Section: Discussionmentioning

confidence: 76%

Infections caused byescherichia coliresistant to norfloxacin in hospitalized cirrhotic patients

Ortiz¹,

Vila²,

Soriano³

et al. 1999

Hepatology

112

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Selective intestinal decontamination with norfloxacin is useful to prevent bacterial infections in several groups of cirrhotic patients at high risk of infection. However, the emergence of infections caused by Escherichia coli resistant to quinolones has recently been observed in cirrhotic patients undergoing prophylactic norfloxacin. Our aim is to determine the characteristics of the infections caused by E. coli resistant to norfloxacin in hospitalized cirrhotic patients. One hundred and six infections caused by E. coli in 99 hospitalized cirrhotic patients were analyzed and distributed into two groups: group I (n ‫؍‬ 67), infections caused by E. coli sensitive to norfloxacin, and group II (n ‫؍‬ 39), infections caused by E. coli resistant to norfloxacin. The clinical and analytical characteristics at diagnosis of the infection were similar in both groups. Previous prophylaxis with norfloxacin was more frequent in group II (15/67, 22.4% vs. 32/39, 82%, P F .0001), as a result of a higher number of patients submitted to continuous long-term prophylaxis in this group, whereas previous short-term prophylaxis was similar in both groups. Infections were more frequently nosocomial-acquired in group II than in group I (17/67, 25.3% vs. 20/39, 51.2%, P ‫؍‬ .01). The type of infections was similar in both groups: urinary tract infections 38 in group I and 24 in group II, spontaneous bacterial peritonitis 8 and 2, spontaneous bacteremia 4 and 4, and bacterascites 1 and 0, respectively (pNS). Mortality during hospitalization was similar in the two groups (4/67, 5.9% vs. 5/39, 12.8%, pNS). None of the E. coli resistant to norfloxacin were also resistant to cefotaxime and only one of them was resistant to amoxicillin-clavulanic acid. Prophylaxis with norfloxacin, usually continuous long-term prophylaxis, favors the development of infections caused by norfloxacin-resistant E. coli. Long-term antibiotic prophylaxis should therefore be restricted to highly selected groups of cirrhotic patients at high-risk of infection. Infections caused by E. coli resistant to norfloxacin show a severity similar to those caused by sensitive E. coli. No significant associated resistance between norfloxacin and the antibiotics most frequently used in the treatment of bacterial infections in cirrhotic patients has been observed.

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“…41 The major concern with the use of prolonged antibiotic prophylaxis is that it will lead to selection of antibioticresistant bacteria. 42,43 Recent studies have shown that bacterial overgrowth and bacterial translocation can also be decreased in experimental cirrhosis by accelerating intestinal transit with cisapride 14 or with propranolol. 44 However, cisapride can produce QT interval prolongation and ventricular arrhythmias.…”

Section: Discussionmentioning

confidence: 99%

Oral bile acids reduce bacterial overgrowth, bacterial translocation, and endotoxemia in cirrhotic rats

et al. 2003

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Experiments were performed to test whether conjugated bile acid administration would decrease bacterial overgrowth, bacterial translocation, and endotoxemia in ascitic cirrhotic rats. Cholylsarcosine, a deconjugation-dehydroxylation resistant and cholylglycine, a deconjugation-dehydroxylation susceptible bile acid were used. Rats with CCl 4 -induced cirrhosis and ascites were fed cholylsarcosine, cholylglycine (both at 70 mg/kg/d), or placebo for 2 weeks. Healthy rats, as controls, were treated similarly. In cirrhotic rats receiving placebo, bile secretion from an acute biliary fistula was lower than in healthy rats (27.2 ؎ 6.5 vs. 53.0 ؎ 3.1 L/kg/min; mean ؎ SE, P < .05). The administration of conjugated bile acids to cirrhotic rats normalized bile secretion (cholylsarcosine, 51.8 ؎ 6.29; cholylglycine, 52.72 ؎ 8.9 L/kg/min). Total ileal bacterial content was 6-fold higher in ascitic cirrhotic rats than in healthy rats. Conjugated bile acid administration reduced bacterial content to normal levels. Bacterial translocation was less in cirrhotic animals receiving conjugated bile acids (cholylsarcosine, 33%; cholylglycine, 26%) than in animals receiving placebo (66%). Endotoxemia was decreased in cirrhotic rats by conjugated bile acid feeding (cholylsarcosine, 0.098 ؎ 0.002; cholylglycine 0.101 ؎ 0.007 EU/mL) compared with placebo (0.282 ؎ 0.124, P < .001). Survival was greater in animals receiving conjugated bile acids (cholylsarcosine, 10/15; cholylglycine, 11/15; placebo, 5/15). In conclusion, the administration of conjugated bile acids to ascitic cirrhotic rats increased bile acid secretion, eliminated intestinal bacterial overgrowth, decreased bacterial translocation, decreased endotoxemia, and increased survival. Oral conjugated bile acids may be useful in preventing bacterial translocation, endotoxemia, and spontaneous bacterial perotonitis in cirrhotic patients. (HEPATOLOGY 2003;37:551-557.)

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Effect of cisapride on intestinal bacterial overgrowth and bacterial translocation in cirrhosis

Cited by 163 publications

References 37 publications

Peripheral blood mononuclear cell expression of toll-like receptors and relation to cytokine levels in cirrhosis

Peripheral blood mononuclear cell expression of toll-like receptors and relation to cytokine levels in cirrhosis

Infections caused byescherichia coliresistant to norfloxacin in hospitalized cirrhotic patients

Oral bile acids reduce bacterial overgrowth, bacterial translocation, and endotoxemia in cirrhotic rats

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