Resection of a methicillin-resistant Staphylococcus aureus liver abscess in a patient with Crohn's disease under infliximab treatment: a case report.

INTRODUCTION: A liver abscess in Crohn's disease is a rare but important entity that is associated with a poor prognosis and high mortality when treatment is delayed. We report a case of successful liver segmentectomy for a methicillin-resistant Staphylococcus aureus liver abscess in a patient with Crohn's disease under infliximab treatment. CASE PRESENTATION: A 31-year-old Japanese man, who had been treated with infliximab infusions for Crohn's disease, was referred to our hospital presenting with an abrupt onset of high fever and an elevated white blood cell count and serum C-reactive protein level. Computed tomography revealed a liver abscess occupying segment 8. The limited effect of percutaneous transhepatic abscess drainage and antibiotics led us to perform radical resection of the abscess. The patient recovered quickly after surgery and the postoperative course was uneventful. CONCLUSION: The present case suggests that surgical removal of an abscess should be considered for patients under immunosuppression or refractory to conventional treatment.

Application of fluorescent cholangiography to single-incision laparoscopic cholecystectomy.

BACKGROUND: Although the use of single-incision laparoscopic cholecystectomy (SILC) is spreading rapidly, this technique has disadvantages. It does not allow for sufficient surgical views to be obtained or for intraoperative radiographic cholangiography to be performed. Fluorescent cholangiography using a preoperative intravenous injection of indocyanine green (ICG) may be useful for identifying the biliary tract during both SILC and conventional laparoscopic cholecystectomy. METHODS: For seven patients undergoing SILC, 1 ml of ICG (2.5 mg) was administered by intravenous injection before the surgery. The prototype fluorescent imaging system consisted of a xenon light source and a 30° laparoscope (diameter, 10 mm) equipped with a charge-coupled device camera capable of filtering out light with wavelengths shorter than 810 nm. The laparoscope was introduced through an umbilical trocar. Fluorescent cholangiography then was performed by changing the color images to fluorescent images using a foot switch during dissection of the triangle of Calot. RESULTS: Fluorescent cholangiography identified the confluence between the cystic duct and the common hepatic duct in all seven patients before and throughout the dissection of the triangle of Calot. The interval from the injection of ICG to the first obtained fluorescent cholangiography before dissection of the triangle of Calot ranged from 35 to 75 min. CONCLUSIONS: Fluorescent cholangiography enabled real-time identification of the extrahepatic bile ducts during SILC without necessitating catheterization of the bile duct. Such properties of fluorescent cholangiography are expected to be helpful for ensuring the safety of SILC and expanding the indications for the procedure.

Human serum albumin as an antioxidant in the oxidation of (-)-epigallocatechin gallate: participation of reversible covalent binding for interaction and stabilization.

Human serum albumin (HSA) contributes to the stabilization of (-)-epigallocatechin gallate (EGCg) in serum. We characterize in the present study the mechanisms for preventing EGCg oxidation by HSA. EGCg was stable in human serum or buffers with HSA, but (-)-epigallocatechin (EGC) was unstable. We show by comparing EGCg and EGC in a neutral buffer that EGCg had a higher binding affinity than EGC. This indicates that the galloyl moiety participated in the interaction of EGCg with HSA and that this interaction was of critical importance in preventing EGCg oxidation. The binding affinity of EGCg for HSA and protein carbonyl formation in HSA were enhanced in an alkaline buffer. These results suggest the reversible covalent modification of EGCg via Schiff-base formation, and that the immobilization of EGCg to HSA, through the formation of a stable complex, prevented the polymerization and decomposition of EGCg in human serum.

Structural characteristics of green tea catechins for formation of protein carbonyl in human serum albumin.

Catechins are polyphenolic antioxidants found in green tea leaves. Recent studies have reported that various polyphenolic compounds, including catechins, cause protein carbonyl formation in proteins via their pro-oxidant actions. In this study, we evaluate the formation of protein carbonyl in human serum albumin (HSA) by tea catechins and investigate the relationship between catechin chemical structure and its pro-oxidant property. To assess the formation of protein carbonyl in HSA, HSA was incubated with four individual catechins under physiological conditions to generate biotin-LC-hydrazide labeled protein carbonyls. Comparison of catechins using Western blotting revealed that the formation of protein carbonyl in HSA was higher for pyrogallol-type catechins than the corresponding catechol-type catechins. In addition, the formation of protein carbonyl was also found to be higher for the catechins having a galloyl group than the corresponding catechins lacking a galloyl group. The importance of the pyrogallol structural motif in the B-ring and the galloyl group was confirmed using methylated catechins and phenolic acids. These results indicate that the most important structural element contributing to the formation of protein carbonyl in HSA by tea catechins is the pyrogallol structural motif in the B-ring, followed by the galloyl group. The oxidation stability and binding affinity of tea catechins with proteins are responsible for the formation of protein carbonyl, and consequently the difference in these properties of each catechin may contribute to the magnitude of their biological activities.

Expression of transforming growth factor-alpha and -beta in hepatic lobes after hemihepatic portal vein embolization.

Hemihepatic portal vein embolization (PVE) concomitantly induces atrophy in embolized and compensatory hypertrophy in nonembolized hepatic lobes. The aim of the present study was to evaluate the involvement of growth stimulatory and inhibitory factors in these hepatic lobes after PVE. Liver specimens from the embolized and nonembolized lobes of ten patients who underwent hepatectomy (8-22 days) after undergoing PVE were obtained. Proliferation and apoptosis were examined immunohistochemically using Ki-67 and the Tdt-mediated dUTP-biotin nick end-labeling method. The expression of transforming growth factor-alpha (TGF-alpha) and transforming growth factor-beta (TGF-beta) was also examined by immunohistochemical staining. PVE induced hepatocyte apoptosis in the embolized lobe and hepatocyte proliferation in the nonembolized lobe. TGF-alpha expression in the hepatocytes of the nonembolized lobe was markedly increased, whereas TGF-alpha was also overexpressed, albeit moderately, in the embolized lobe. In contrast, TGF-beta expression in the hepatocytes of the embolized lobe was significantly increased, and TGF-beta expression was also increased, although to a lesser extent, in the nonembolized lobe. The degree of volume changes of the nonembolized lobe and the embolized lobe after PVE was statistically correlated with the ratios of TGF-alpha and TGF-beta expression in these lobes (r = 0.886, P < .0001). In conclusion, these findings indicate that TGF-alpha and TGF-beta expression (assessed by immunohistochemical staining) increase in relation to hepatocyte proliferation and apoptosis, respectively, after PVE in humans and the balance of the two factors may contribute to hepatic atrophy and hypertrophy concomitantly observed in this model.

Factors affecting liver regeneration after right portal vein embolization.

BACKGROUND/AIMS: The factors influencing the effect of portal vein embolization performed prior to hepatectomies are not clearly understood. METHODOLOGY: In 18 patients who underwent portal vein embolization, serum transforming growth factor-alpha levels and the nonembolized liver volume were studied after portal vein embolization. The increase in the nonembolized liver volume was compared with the change in serum transforming growth factor-alpha levels and several other clinical variables. RESULTS: The volume of the nonembolized liver significantly increased from 430+/-114 cm3 to 521+/-113 cm3. The serum transforming growth factor-alpha levels significantly increased on the 7th day after portal vein embolization and peaked on the 18th day. The percentage increase in the nonembolized liver volume 14 days after portal vein embolization was significantly correlated with the nonembolized liver volume and the increase in the portal flow velocity, and it was independently and significantly correlated with the increase in the transforming growth factor-alpha level 14 days after portal vein embolization (r2=0.674, P=0.0014 and r=0.761, P<0.0005). CONCLUSIONS: The increase in the transforming growth factor-alpha level 14 days after portal vein embolization was the only independent factor related to the hypertrophy of the nonembolized liver. Measurement of its serum level may be a useful indicator in the scheduling of subsequent extensive hepatectomies.

Immunosuppressive effect of chenodeoxycholic acid on natural killer cell activity in patients with biliary atresia and hepatitis C virus-related liver cirrhosis.

Patients with severe liver diseases, such as liver cirrhosis and biliary atresia, have low natural killer (NK) cell activity. The relations between NK activity and measures of liver function, including serum levels of total bilirubin, total bile acids, bile acid components, aspartate aminotransferase, and alanine aminotransferase, and platelet count were examined in patients with biliary atresia (6 boys and 6 girls; mean age, 4.8+/-5.7 years) and patients with liver cirrhosis due to hepatitis C virus infection (10 men and 2 women; mean age, 54.3+/-13.8 years). Univariate analysis showed that platelet count was positively correlated with NK activity in patients with biliary atresia (r = 0.611, P < 0.05). Serum levels of free chenodeoxycholic acid were negatively correlated with NK activity both in patients with biliary atresia (r = -0.647, P < 0.05) and in patients with hepatitis C virus-related liver cirrhosis (r = -0.876, P < 0.01). None of the other free bile acids or conjugated bile acids or other indicators of liver function were correlated with NK activity. Multiple stepwise regression analysis showed that only levels of free chenodeoxycholic acid were independently correlated with NK activity. All patients with biliary atresia underwent liver transplantation from living related donors. NK activity had increased significantly two months after transplantation (from 24.1+/-20.2% to 49.2+/-12.5%, P < 0.01). In contrast, levels of free chenodeoxycholic acid in transplant recipients had decreased significantly two months after transplantation (from 1.22+/-1.16 to 0.26+/-0.21 micromol/l, P < 0.05). In conclusion, in patients with biliary atresia or liver cirrhosis, NK activity in peripheral blood decreases, mostly because of free chenodeoxycholic acid.