The soluble mannose receptor is released from the liver in cirrhotic patients, but is not associated with bacterial translocation.

BACKGROUND & AIMS: Intestinal bacterial translocation is involved in activation of liver macrophages in cirrhotic patients. Macrophages play a key role in liver inflammation and are involved in the pathogenesis of cirrhosis and complications. Bacterial translocation may be determined by presence of bacterial DNA and macrophage activation, by the soluble mannose receptor. We hypothesize that the soluble mannose receptor is released from hepatic macrophages in cirrhosis and associated with bacterial DNA, portal pressure and complications. METHODS: We investigated 28 cirrhotic patients set for transjugular intrahepatic portosystemic shunt insertion as a result of refractory ascites (n=17), acute (n=3), or recurrent variceal bleeding (n=8). We analysed plasma from the portal and hepatic veins for bacterial DNA and soluble mannose receptor with qPCR and ELISA. RESULTS: The median soluble mannose receptor level was elevated in the hepatic vein compared with the portal vein (0.57(interquartile range 0.31) vs 0.55(0.40) mg/L, P=.005). The soluble mannose receptor levels were similar in bacterial DNA-positive and -negative patients. The soluble mannose receptor level in the portal and hepatic veins correlated with the portal pressure prior to transjugular intrahepatic portosystemic shunt insertion (r=.52, P<.008, both) and the levels correlated with Child-Pugh score (r=.63 and r=.56, P<.004, both). We observed higher soluble mannose receptor levels in patients with acute variceal bleeding compared to other indications (P<.05). CONCLUSION: This study showed hepatic soluble mannose receptor excretion with a higher level in the hepatic than the portal vein, though with no associations to bacterial DNA. We observed associations between soluble mannose receptor levels and portal pressure and higher levels in patients with acute variceal bleeding indicating the soluble mannose receptor as a marker of complications of cirrhosis, but not bacterial translocation.

[Colectomy in a patient with pneumatosis coli]. / Kolektomi hos en patient med pneumatosis coli

Pneumatosis coli (PC) is a rare condition which may be difficult to diagnose. We report a case of PC in a 46-year-old woman, where colonoscopy and biopsies showed signs of widespread polyposis. She had a prophylactic colectomy. Pathologic examination of the specimen showed multiple air-filled cysts in the colonic wall. By analysis of a preoperative abdominal computed tomography with lung window the cysts could be visualised. This procedure could be a valuable diagnostic tool for excluding PC in patients suspected for polyposis, but with a negative family history of familial adenomatous polyposis.

No difference in portal and hepatic venous bacterial DNA in patients with cirrhosis undergoing transjugular intrahepatic portosystemic shunt insertion.

BACKGROUND: Bacterial translocation (BT) with immune activation may lead to hemodynamical alterations and poor outcomes in patients with cirrhosis. AIMS: We investigated bacterial DNA (bDNA), a marker of BT, and its relation to portal pressure and markers of inflammation in the portal and hepatic veins in patients with cirrhosis undergoing TIPS insertion. METHODS: We analysed plasma for bDNA and markers of inflammation in 28 patients [median portal pressure gradient 15 (11-19) mmHg] during TIPS treatment for refractory ascites (n = 19) or acute variceal bleeding (n = 9). Advanced cirrhosis was present in the majority [Child-Pugh class (A/B/C): 1/14/13], and most often caused by alcohol (n = 21). RESULTS: bDNA was detectable in one or both samples in 16 of 28 patients (57%). bDNA was present in 39% of the samples from the portal vein vs 43% of the samples in the hepatic vein (P = 0.126). Antibiotics had no effect on bDNA or markers of inflammation. Markers of inflammation did not differ between the hepatic and portal veins with the exceptions of soluble urokinase plasminogen activating receptor (suPAR) and vascular endothelial growth factor (VEGF), both higher in the hepatic vein (P = 0.031 and 0.003 respectively). CONCLUSIONS: No transhepatic gradient of bDNA was evident, suggesting that no major hepatic elimination of bDNA occurs in advanced liver disease. bDNA, in contrast to previous reports was largely unrelated to a panel of markers of inflammation and without relation to portal pressure.

Small intestinal transit in patients with liver cirrhosis and portal hypertension: a descriptive study.

BACKGROUND: Gastrointestinal dysmotility may be involved in the development of bacterial translocation and infection in patients with liver cirrhosis. The aim of the present study was to describe gastric, small intestinal and colorectal motility and transit in patients with liver cirrhosis and portal hypertension using a magnet-based Motility Tracking System (MTS-1) and standard radiopaque markers. METHODS: We included 15 patients with liver cirrhosis (8 Child-Pugh A, 6 Child-Pugh B, and 1 Child-Pugh C) and portal hypertension (11 males, median age 54 years (range 38-73), median hepatic venous pressure gradient 18 mmHg (range 12-37)), and 18 healthy controls (8 males, median age 58 years (range 34-64)). The gastric emptying time and small intestinal motility were evaluated by MTS-1, and the total gastrointestinal transit time was assessed by radiopaque markers and abdominal radiographs. RESULTS: The velocity through the proximal small intestine was significantly higher in cirrhotic patients (median 1.27 metres (m)/hour, range 0.82-2.68) than in the healthy controls (median 1.00 m/hour, range 0.46-1.88) (p = 0.03). Likewise, the magnet travelled significantly longer in both fast (p = 0.04) and slow movements (p = 0.05) in the patient group. There was no significant difference in either gastric emptying time--23 minutes (range 5-131) in patients and 29 minutes (range 10.5-182) in healthy controls (p = 0.43)--or total gastrointestinal transit time--1.6 days (range 0.5-2.9) in patients and 2.0 days (range 1.0-3.9) in healthy controls (p = 0.33). No correlation was observed between the hepatic venous pressure gradient and the velocity of the magnet through the small intestine. CONCLUSION: Patients with liver cirrhosis and portal hypertension demonstrated faster-than-normal transit through the proximal small intestine. This may be due to an overactive bowel, as suggested by previous studies.

[Chronic Budd-Chiari syndrome can cause liver cirrhosis]. / Kronisk Budd-Chiaris syndrom kan være årsag til levercirrose.

Budd-Chiari syndrome (BCS) is a rare disease defined by congestive hepatopathy with obstruction of the hepatic venous outflow tract. Classical symptoms and signs include ascites, hepatomegaly, abdominal pain and various degrees of liver dysfunction. BCS is predominantly caused by thrombosis, malformations and venous compression. We present a case, in which BCS was the cause of liver cirrhosis complicated with refractory ascites and which can be misinterpreted as hepatocellular carcinoma nodules. The diagnosis was confirmed during the transjugular intrahepatic portosystemic shunt procedure with successful vascular stenting resolving the ascites formation.