Small Intestinal Motility Disturbances and Bacterial Overgrowth in Patients With Liver Cirrhosis and Portal Hypertension

Gunnarsdóttir, Steingerður Anna; Sadik, Riadh; Shev, Steven; Simrén, Magnus; Sjövall, Henrik; Stotzer, Per-Ove; Abrahamsson, Hasse; Olsson, Rolf; Bjõrnsson, Einar

doi:10.1111/j.1572-0241.2003.07475.x

Cited by 159 publications

(74 citation statements)

References 31 publications

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“…Therefore, reduction of PH is expected to increase hepatic processing of IgAIC. PH also decreases small intestinal motility promoting bacterial overgrowth [31,32] , while in the same time increases intestinal permeability [33] . In this regard, increased circulating IgA and IgAIC may represent an exaggerated response of immune system to excess gut antigen exposure [34,35] , resulting from diminished mucosal integrity and spillage of IgA into the circulation.…”

Section: Discussionmentioning

confidence: 99%

Association of liver cirrhosis related IgA nephropathy with portal hypertension

Kalambokis

Christou²,

Stefanou³

et al. 2007

WJG

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A high incidence of IgA nephropathy has been reported in patients with liver cirrhosis, though, clinically evident nephrotic syndrome is very uncommon. Impaired hepatic clearance of circulating IgA immune complexes and subsequent deposition in renal glomeruli has been considered principally in the pathogenesis of liver cirrhosis associated IgA nephropathy. Here we report on a patient with cryptogenic liver cirrhosis and splenic vein thrombosis, who presented with nephrotic syndrome. Renal biopsy showed findings consistent with IgA nephropathy. Lower endoscopy showed features of portal hypertensive colopathy. Following initiation of propranolol and anticoagulant treatment to reduce portal pressure, a gradual decrease of proteinuria and hematuria to normal range was noted. The potential p a t h o g e n e t i c ro l e o f p o r t a l hy p e r t e n s i o n i n t h e development of IgA nephropathy in cirrhotic patients is discussed.

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Section: Discussionmentioning

confidence: 99%

Association of liver cirrhosis related IgA nephropathy with portal hypertension

Kalambokis

Christou²,

Stefanou³

et al. 2007

WJG

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“…Complications such as SBP occur long after development of frank cirrhosis, and bacterial overgrowth due to compromised intestinal motility may facilitate translocation in SBP. 41,42 A number of factors may play a role in mediating bacterial translocation across the intestine during liver cirrhosis. These include (1) damage to the intestinal mucosa; (2) changes on the surfactant and brush border membranes lining the lumen of the gut, making them amenable to bacterial adhesion; and (3) changes in the luminal gut flora, which might alter adherence to the mucosa.…”

Section: Discussionmentioning

confidence: 99%

Intestinal mucosal alterations in rats with carbon tetrachloride-induced cirrhosis: Changes in glycosylation and luminal bacteria

et al. 2006

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Spontaneous bacterial peritonitis is a major cause of mortality after liver cirrhosis. Altered permeability of the mucosa and deficiencies in host immune defenses through bacterial translocation from the intestine due to intestinal bacterial overgrowth have been implicated in the development of this complication. Molecular mechanisms underlying the process are not well known. In order to understand mechanisms involved in translocation of bacteria, this study explored the role of oxidative stress in mediating changes in intestinal mucosal glycosylation and luminal bacterial content during cirrhosis. CCl 4 -induced cirrhosis in rats led to prolonged oxidative stress in the intestine, accompanied by increased sugar content of both intestinal brush border and surfactant layers. This was accompanied by changes in bacterial flora in the gut, which showed increased hydrophobicity and adherence to the mucosa. Inhibition of xanthine oxidase using sodium tungstate or antioxidant supplementation using vitamin E reversed the oxidative stress, changes in brush border membrane sugar content, and bacterial adherence. In conclusion, oxidative stress in the intestine during cirrhosis alters mucosal glycosylation, accompanied by an increased hydrophobicity of luminal bacteria, enabling increased bacterial adherence onto epithelial cells. This might facilitate translocation across the mucosa, resulting in complications such as spontaneous bacterial peritonitis. (HEPATOLOGY 2006;43:837-846.)

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“…30 In a clinical study of 24 patients with liver cirrhosis the bacterial overgrowth was enhanced by portal hypertension, as suggested by animal models. 31 In addition progressive intestinal dysbiosis was identified in patients with LC especially in advanced stages of the disease. 32 Interestingly, drugs that may alter the microbiota (i.e proton pomp inhibitors) or that affect the intestinal mobility (b-blockers) can have a role modifying the rate of bacterial infections in this setting.…”

Section: Pathophysiology Of Bsis In Patients With Liver Cirrhosis: Inmentioning

confidence: 99%

Bloodstream infections in patients with liver cirrhosis

et al. 2016

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Bloodstream infections are a serious complication in patients with liver cirrhosis. Dysregulated intestinal bacterial translocation is the predominant pathophysiological mechanism of infections in this setting. For this reason enteric Gram-negative bacteria are commonly encountered as the first etiological cause of infection. However, through the years, the improvement in the management of cirrhosis, the recourse to invasive procedures and the global spread of multidrug resistant pathogens have importantly changed the current epidemiology. Bloodstream infections in cirrhotic patients are characterized by high mortality rate and complications including metastatic infections, infective endocarditis, and endotipsitis (or transjugular intrahepatic portosystemic shunt-related infection). For this reason early identification of patients at risk for mortality and appropriated therapeutic management is mandatory. Liver cirrhosis can significantly change the pharmacokinetic behavior of antimicrobials. In fact hypoproteinaemia, ascitis and third space expansion and impairment of renal function can be translated in an unpredictable drug exposure.

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Small Intestinal Motility Disturbances and Bacterial Overgrowth in Patients With Liver Cirrhosis and Portal Hypertension

Abstract: Abnormal small bowel motility and SIBO is common in patients with liver cirrhosis with concomitant portal hypertension. Portal hypertension per se might be significantly related to small bowel abnormalities observed in patients with liver cirrhosis.

Cited by 159 publications

References 31 publications

Association of liver cirrhosis related IgA nephropathy with portal hypertension

Association of liver cirrhosis related IgA nephropathy with portal hypertension

Intestinal mucosal alterations in rats with carbon tetrachloride-induced cirrhosis: Changes in glycosylation and luminal bacteria

Bloodstream infections in patients with liver cirrhosis

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