[Pancreatobiliary Fistula with Jaundice-A Case Report].

An 80-year-old woman was admitted to our hospital due to jaundice. CT and MRCP revealed that the common bile duct and main pancreatic duct were dilatated due to a cystic lesion in the pancreatic head. Moreover, ERCP revealed the presence of a pancreatobiliary fistula and mucus discharge from the enlarged papilla. The patient underwent biliary and pancreatic drainage using plastic stents. However, the treatment was not effective because of the presence of the protein plug. The patient underwent EST because of her rejection to surgery. After the procedure, jaundice was resolved. We report this case with a review of the available literature.

Validation of thermally assisted hydrolysis and methylation-gas chromatography for rapid and direct compositional analysis of poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) in whole bacterial cells.

Thermally assisted hydrolysis and methylation-gas chromatography (THM-GC) in the presence of an organic alkali was validated for the compositional analysis of poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) [P(3HB-co-3HHx)] accumulated in whole bacterial cells. Recombinant Cupriavidus necator Re2058/pCB113 was grown in a batch fermentation with different concentration of palm oil and fructose in order to control the molar fraction of 3HHx in P(3HB-co-3HHx) produced in the cells. Trace amounts (30µg) of freeze-dried cells were directly subjected to THM-GC in the presence of tetramethylammonium hydroxide (TMAH) at 400°C. The obtained chromatograms clearly showed nine characteristic peaks, attributed to the THM products from 3HB and 3HHx units in the polymer chains, without any appreciable interference by the bacterial matrix components. Based on these peak intensities, the copolymer compositions were determined rapidly without using any cumbersome and lengthy sample pretreatment as in conventional GC method. Moreover, the compositions thus obtained were strongly correlated with those by NMR and conventional GC involving solvent extraction.

Upper gastrointestinal bleeding in patients receiving dual antiplatelet therapy after coronary stenting.

OBJECTIVE: We investigated the risk of upper gastrointestinal (UGI) bleeding and the protective effect of concomitant anti-secretory drugs during dual antiplatelet therapy administered following implantation of drug-eluting stents (DES) for coronary heart disease. Because proton pump inhibitors (PPIs) are reported to decrease the platelet inhibitory effects of clopidogrel, we also assessed cardiovascular outcomes in patients taking thienopyridine derivatives with or without anti-secretory drug. METHODS: We retrospectively analyzed 243 patients, who underwent DES implantation between January 2006 and December 2007 and were receiving dual anti-platelet therapy post-surgery. The main outcome measurement was the presence of UGI bleeding. Cardiovascular outcomes were assessed by follow-up coronary angiography (CAG) findings. Data were collected from medical records. RESULTS: Eight cases of UGI bleeding were observed during the follow-up period, none of whom were taking anti-secretory drugs. Among the 243 cases, 108 cases were taking anti-secretory drugs: a PPI (67 cases), and an H2 receptor antagonist (41 cases). No UGI bleeding was observed among patients who were taking concomitant anti-secretory drugs. The 1- and 2-year cumulative incidences of UGI bleeding among patients who were not taking anti-secretory drugs were 4.5% and 9.2%, respectively. When CAG findings were compared between patients not taking any anti-secretory drug, taking PPI, or taking H2RA, significantly more stenotic lesions of the coronary artery were observed in the PPI-treatment group. CONCLUSION: Concomitant use of an anti-secretory agent was associated with a reduced risk of UGI bleeding. Use of PPI may be associated with an attenuation of the effect of dual antiplatelet therapy.

Plasma exchange in combination with online-hemodiafiltration as a promising method for purifying the blood of fulminant hepatitis patients.

BACKGROUND: Fulminant hepatitis is an intractable disease caused by various etiological agents. Artificial liver support (ALS) is a symptomatic treatment used to control serious symptoms, such as bleeding tendency, hepatic coma, and brain edema. METHODS: The present study involved four patients with fulminant hepatitis who were admitted to Showa University Fujigaoka Hospital between January 2007 and June 2007. All four patients were subacute type disease of indeterminate etiology. The four patients were placed on an ALS system that comprised plasma exchange and online hemodiafiltration. The effect of the ALS on various symptoms of fulminant hepatitis was evaluated, and the levels of glutamine in the patients' plasma samples and the discarded buffer were assayed using automatic analyser. RESULTS: Three of the four patients regained full consciousness and survived. The remaining patient died despite recovering from hepatic coma with ALS. The plasma glutamine levels were significantly reduced by artificial liver support. The estimated distribution volume of removed Gln ranged from 30 L to 60 L. CONCLUSIONS: Plasma exchange in combination with online hemodiafiltration is a promising and effective method for purifying the blood of patients with fulminant hepatitis.

Possible association of vigorous hepatitis B virus replication with the development of fulminant hepatitis.

A 49 year-old man was referred to our hospital for fear of developing fulminant hepatic failure. There had been an outbreak of fulminant hepatitis B in a dialysis clinic in the western part of Honshu, Japan, that resulted in four deaths among six patients. After the sixth patient contracted severe hepatitis, all patients in the unit were screened biweekly for hepatitis B surface antigen (HBsAg) to detect newly infected patients as soon as possible. Our patient was the seventh victim, and on the day he gave a positive result for HBsAg, his hepatitis B virus (HBV) DNA level had reached 1.1 x 10(11) copies/ml as assessed by real time polymerase chain reaction. Sequence analysis of the causal HBV revealed the presence of a mutation in the precore region (nt 1896), two mutations in the core promoter (nt 1762 and nt 1764), and some minor mutations in the P gene that were restricted to the upstream region. These mutations are indicative of a virus with a high replicative rate that cannot secrete HBeAg. Taken together, these findings indicate that it is very likely that the replicative ability of the causal virus was as vigorous as that of HBV in hepatitis B e antigen-positive asymptomatic carriers with markedly high viral titers. The present case report provides clinical evidence of a possible association between the rapid spread of highly replicative HBV before host immunological recognition and the development of fulminant hepatitis.

Acute necrotizing esophagitis: role of nonsteroidal anti-inflammatory drugs.

BACKGROUND: Acute necrotizing esophagitis (ANE) is a rarely described entity that is thought to be a cause of upper gastrointestinal (UGI) bleeding, The present study examined the incidence of ANE among patients with UGI bleeding, as well as the clinical features of ANE, and the coexisting illnesses and medication histories of ANE patients. METHODS: A retrospective analysis of clinical and endoscopic findings and the clinical course in 16 patients with ANE was carried out over a 3-year period. RESULTS: We observed 16 patients (6%) of ANE in 239 patients with UGI bleeding during the 3-year period. The average age of the patients was 62.5 years. The lesions predominantly affected the lower third of the esophagus, and hiatal hernia was the most common (63%) coexisting endoscopic finding. All patients had coexisting disease. Fifty percent of patients with ANE (eight patients) had taken nonsteroidal anti-inflammatory drugs (NSAIDs). ANE also occurred in four patients with diabetic ketoacidosis. Supportive therapy, including parenteral nutrition and administration of a proton pump inhibitor, was effective. CONCLUSIONS: ANE is more common than has been previously reported, and it should be included in the differential diagnosis of UGI bleeding. ANE could be characterized as an "acute esophageal mucosal lesion," particularly in aged patients with hiatal hernia and among those who consume NSAIDs.

Elevated cyclooxygenase-2 expression in patients with early gastric cancer in the gastric pylorus.

BACKGROUND: Duodenogastric reflux after surgery increases the risk of gastric carcinoma. To determine whether bile reflux influences the development of gastric cancer in patients who have not had surgery, we compared cyclooxygenase-2 (COX-2) immunoreactivity in early gastric cancer originating from the gastric pylorus and that originating from other locations. We also examined the effects of bile acids on the expression and activity of COX-2 in gastric cells in vitro. METHODS: Tumor sections from 79 patients who underwent endoscopic mucosal resection for early intestinal-type gastric carcinoma were stained using a COX-2-specific monoclonal antibody. Immunoblotting of COX-2 was used to assess the effects of bile acids on COX-2 expression and activity in human gastric cell lines. RESULTS: Among the 79 early gastric cancer lesions studied, 13 (16%) arose in the gastric pylorus. In this group, COX-2 immunoreactivity was negative to weak in 38% (5 of 13 lesions) and moderate to strong in 62% (8 of 13 lesions). In the control group, COX-2 immunoreactivity was negative to weak in 70% (46 of 66 lesions) and moderate to strong in 30% (20 of 66 lesions). COX-2 expression was significantly elevated in early gastric cancer located in the gastric pylorus, compared with that in the other locations. In human gastric cell lines, bile acids induced COX-2 expression, mediated by the ERK 1/2 mitogen-activated protein kinase pathway. CONCLUSIONS: COX-2 expression is elevated in early gastric cancer of the gastric pylorus, a common site of gastric cancer. Bile acids induced COX-2 expression in human gastric cell lines, suggesting a role of bile reflux in gastric carcinogenesis.

Combined interferon alpha2b and cyclosporin A in the treatment of chronic hepatitis C: controlled trial.

BACKGROUND: Only 15% to 20% of patients with chronic hepatitis C have a sustained virological response to interferon monotherapy. The aim of the present study was to compare the efficacy and safety of interferon, in combination with oral cyclosporin A, with interferon monotherapy in the treatment of chronic hepatitis C. METHODS: We assigned 120 patients with chronic hepatitis C to receive the standard Japanese dose of interferon alpha2b alone for 24 weeks or that dose of interferon alpha2b in combination with cyclosporin A, at doses of 200 mg daily for the first 4 weeks and 100 mg daily for the following 20 weeks. All patients were assessed for drug safety, tolerance, and efficacy at the end of weeks 4, 12, 24, and 48. Efficacy was assessed by the disappearance of serum hepatitis C virus (HCV)-RNA by polymerase chain reaction and normalization of serum aminotransferase. The primary endpoint was a sustained virological response; i.e., sustained undetectable serum HCV RNA at 48 weeks. RESULTS: The sustained virological response rate was significantly higher in the combination therapy group (42/76) than in the monotherapy group (14/44; P = 0.01). The sustained biochemical response rate was also higher in the combination therapy group (46/76) than in the monotherapy group (17/44; P = 0.017). In patients with genotype 1 and high viral loads, the sustained virological response rate was markedly higher in the combination therapy group (16/38) than in the monotherapy group (1/21; P = 0.006). Side-effect profiles were similar in the two groups. CONCLUSIONS: In patients with chronic hepatitis C; combined interferon and cyclosporin A treatment was more effective than interferon monotherapy. The benefit was mostly achieved in patients with a high viral load and HCV genotype 1.

Accurate prediction of fulminant hepatic failure in severe acute viral hepatitis: multicenter study.

BACKGROUND: We have attempted to predict the development of fulminant hepatic failure at the stage of severe acute hepatitis before the onset of coma. This prediction is valuable because it may be used to block the development of fulminant hepatic failure with appropriate medical treatment. METHODS: To establish a discrimination formula, we retrospectively compared 13 clinical and laboratory variables in 36 patients with acute viral hepatitis and prothrombin levels of 40% or less of the control value who later developed fulminant hepatic failure with these variables in 12 patients who recovered spontaneously. A prospective study of 58 patients who developed fulminant hepatic failure and 18 who spontaneously recovered confirmed the validity of this formula. RESULTS: In the retrospective study,we established the following discrimination equation: Z = -0.89 + 1.74 x (causal viruses, 1 point for type A or type B in acute hepatitis B virus [HBV] infection, 2 points for others) + 0.056 x (total bilirubin, mg/dl)-0.014 x (cholinesterase, U/ml). A positive Z value indicates that fulminant hepatic failure will develop. In the prospective study, the specificity, sensitivity, predictive accuracy, and positive and negative predictive values were 0.833, 0.983, 0.947, 0.950, and 0.938, respectively. CONCLUSIONS: The present study indicated that fulminant hepatic failure can be predicted, by a simple discrimination equation, at the stage of severe acute hepatitis.