Clinical significance of methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci colonization in liver transplant recipients

BACKGROUND/AIMS: Liver transplant patients are at high risk for methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci (VRE) colonization. We evaluated patients before and after liver transplant using active surveillance culture (ASC) to assess the prevalence of MRSA and VRE and to determine the effect of bacterial colonization on patient outcome. METHODS: We performed ASC on 162 liver transplant recipients at the time of transplantation and 7 days posttransplantation to monitor the prevalence of MRSA and VRE. RESULTS: A total of 142 patients had both nasal and rectal ASCs. Of these patients, MRSA was isolated from 12 (7.4%) at the time of transplantation (group 1a), 9 (6.9%) acquired MRSA posttransplantation (group 2a), and 121 did not test positive for MRSA at either time (group 3a). Among the three groups, group 1a patients had the highest frequency of developing a MRSA infection (p < 0.01); however, group 2a patients had the highest mortality rate associated with MRSA infection (p = 0.05). Of the 142 patients, VRE colonization was detected in 37 patients (22.8%) at the time of transplantation (group 1b), 21 patients (20%) acquired VRE posttransplantation (group 2b), and 84 patients did not test positive for VRE at either time (group 3b). Among these three groups, group 2b patients had the highest frequency of VRE infections (p < 0.01) and mortality (p = 0.04). CONCLUSIONS: Patients that acquired VRE or MRSA posttransplantation had higher mortality rates than did those who were colonized pre-transplantation or those who never acquired the pathogens. Our findings highlight the importance of preventing the acquisition of MRSA and VRE posttransplantation to reduce infections and mortality among liver transplant recipients.

Epidemiology and Risk Factors for Bacteremia in 144 Consecutive Living-Donor Liver Transplant Recipients

PURPOSE: Bacteremia is a major infectious complication associated with mortality in liver transplant recipients. The causative organisms and clinical courses differ between medical centers due to variations in regional bacterial epidemiology and posttransplant care. Further, living donors in Korea contribute to 83% of liver transplants, and individualized data are required to improve survival rates. PATIENTS AND METHODS: We retrospectively analyzed 104 subjects who had undergone living-donor liver transplant from 2005 to 2007. RESULTS: Among the 144 consecutive living-donor liver transplant recipients, 24% (34/144) developed bacteremia, 32% (46/144) developed non-bacteremic infections, and 44% (64/144) did not develop any infectious complications. Forty episodes of bacteremia occurred in 34 recipients. The major sources of bacteremia were intravascular catheter (30%; 12/40), biliary tract (30%; 12/40), and abdomen (22.5%; 9/40). Gram-positive cocci were more common (57.5%; 23/40) than Gram-negative rods (32.5 %; 13/40) and fungi (10%; 4/40). The data revealed that the following factors were significantly different between the bacteremia, non-bacteremic infection, and no infection groups: age (p = 0.024), posttransplant hemodialysis (p = 0.002), ICU stay (p = 0.012), posttransplant hospitalization (p < 0.0001), and duration of catheterization (p < 0.0001). The risk factors for bacteremia were older than 55 years (odds ratio, 6.1; p = 0.003), catheterization for more than 22 days (odds ratio, 4.0; p = 0.009), UNOS class IIA (odds ratio, 6.6; p = 0.039), and posttransplant hemodialysis (odds ratio, 23.1; p = 0.001). One-year survival rates in the bacteremic, non-bacteremic infection, and no infection groups were 73.2%, 91.3%, and 93.5%, respectively. CONCLUSION: Early catheter removal and preservation of renal function should focus for improving survival after transplant.

Clinical and Biochemical Parameters of Nutrition to Predict Hepatic Encephalopathy in Cirrhotic Patients / 대한소화기학회지

BACKGROUND/AIMS: Protein-calorie malnutrition is a common complication in cirrhosis. Protein restriction for the treatment of hepatic encephalopathy (HE) may cause disease progression and poor prognosis. Therefore, we evaluated important clinical parameters for nutritional state in cirrhotic patients with or without HE to predict the development of HE. METHODS: Twenty-two cirrhotic patients were divided into two groups; group A-13 patients without HE and group B-9 patients with HE. Clinical and biochemical parameters, serum proteins {serum albumin, insulin-like growth factor-1 (IGF-1), transferrin, leptin, etc}, immunologic parameters and anthropometry were measured. RESULTS: Child-Pugh score and Model for End-stage Liver Disease (MELD) scale were higher in group B (p<0.01). After correction of various factors affecting nutritional assessment, especially of Child-Pugh score and MELD scale, leptin was higher in group B (p<0.05). There was no difference in anthropometric measurements. Transferrin correlated inversely with MELD scale in group A (p<0.01). IGF-1 correlated inversely with total lymphocyte count in group B (p<0.05). Leptin correlated with Child-Pugh scores, total lymphocyte count and mid-arm muscle cirumference in group A (p<0.05, p<0.05 and p<0.05, respectively), and correlated inversely with CD8 in group B (p<0.05). CONCLUSIONS: Leptin level is higher in patients with HE, and further studies for parameters of nutrition to predict HE in many cirrhotic patients will be needed.

Electron Microscopic Mesenchymal Response in Chronic Viral Hepatitis / 대한간학회지

BACKGROUND/AIMS: This study was designed to clarify the fine structures of the hepatocytes and mesencymal tissues in chronic hepatitis according to severity. METHOD: For the purpose of elucidating the ultrastructural characteristics of mesenchymal tissues, liver biopsy specimens were studied by light and electron microscopy in 20 patients with chronic hepatitis. RESULTS: 1) Hepatocytes in mesenchymal tissues were thought to be in the stage of regenerated or degenerated process. 2) Regenerating nodules were surrounded by a basement membrane-like materials in the space of Disse. 3) In the widened Disse space the deposition of collagen fiber bundles and increased numbers of hepatic stellate cells in necrotic area were observed. 4) In necrotic areas, hepatic mesenchymal cell response including an increase of collagen fibers and fibroblast, angiogenesis, and a proliferation of bile ductules were also observed. CONCLUSIONS: These observations suggest that the fibrosis in severe chronic hepatitis was accompanied by the mesenchymal response including the proliferation of hepatic stellate cells, fibroblasts, capillarization of Disse space, and mesenchymal proliferation. Finally, this fibrosis observed electron microscopically may be a cause of functional hepatic failure.

Increased Microfilaments in Hepatocytes and Biliary Ductular Cells in Cholestatic Liver Diseases

To assess the extent of microfilaments in cholestatic liver diseases we examined the cytoplasmic microfilaments in intrahepatic and extrahepatic cholestasis in man by electron microscopy. Study subjects were two patients with drug-induced intrahepatic cholestasis, three patients with intrahepatic cholestasis due to viral hepatitis, four patients with extrahepatic cholestasis due to stones of the common bile duct and two patients with primary biliary cirrhosis. Two biopsied specimens from patients without clinical or histological evidence of liver disease served as noncholestatic controls. The microfilaments in hepatocytes and biliary ductular cells were significantly increased in cholestasis compared with those in non-cholestatic controls. Well developed bundles of microfilaments were noted around the pericanalicular ectoplasm and seemed to be parallel to plasma membrane of the hepatocytes in cholestasis. In cholestasis, there were increased bundles of microfilaments around the periluminal region, lateral cell wall, and nucleus of biliary ductular cells. Two patterns of microfilaments bundles (fine microfilamentous network and spindle-shaped dense or clusters of microfilaments) were associated with cholestasis. The clustered form of microfilaments also seemed to be clearly associated with intracytoplasmic vacuoles containing bile salts. In conclusion, the increase of microfilaments in hepatocytes and biliary ductular cells may be the consequence of various forms of cholestasis. Further studies are needed to clarify the functional significance of increased microfilaments in cholestasis.