Predictive Factors for Conversion of Laparoscopic Cholecystectomy

Reliable predictive factors for conversion of laparoscopic cholecystectomy (LC) would be extremely useful in the preparation and planning of admission for patients with symptomatic cholelithiasis. Data from 783 patients in whom LC was attempted in a university clinic from June 1990 to December 1995 were retrospectively analyzed. The aim of this study was to determine preoperative indicators that can be useful for predicting conversion to open cholecystectomy (OC). Conversion was required in 58 (7.4%) patients, of which 48 (83%) were elective and 10 (17%) emergency. Factors evaluated were age, sex, obesity, duration of gallstone disease, co-morbid factors, indication for surgery, previous abdominal surgery, fever, physical examination findings, white blood cell (WBC) count, liver function tests, ultrasound findings, and the experience of the surgeon. Acute cholecystitis, rigidity in the right upper abdomen, fever, thickened gallbladder wall on ultrasonography, elevated alkaline phosphatase (ALP), liver transaminases and the WBC count were significant predictors of conversion in the univariate analysis. Multivariate logistic regression analysis on these significant predictors showed that acute cholecystitis [odds ratio (OR) = 3.12], thickened gallbladder wall on ultrasonography (OR = 3.75), elevated ALP (OR = 2.23), and WBC count (OR = 3.69) were jointly significant.     

Expression of differential nitric oxide synthase isoforms in human normal gastric mucosa and gastric cancer tissue

The present study investigated the expression and distribution of three isoforms of nitric oxide synthase (NOS) in different anatomical regions of the human stomach and in gastric neoplastic tissues by immunohistochemistry using specific antibodies. Intracellular localization of individual isoenzymes of NOS was detected in normal gastric mucosa. Gastric cancer tissues had a marked reduction of all three NOS isoforms expression. The expression of the endothelial NOS, neuronal NOS and inducible NOS in the tumor tissue was significantly lower than in normal gastric mucosa (P = 0.01, P = 0.02, P < 0.01, respectively). In the tumor tissue the expression of inducible NOS was significantly lower than the expression of both constitutive forms of NOS (P < 0.01). There was a tendency to higher expression of both constitutive forms of NOS in earlier stages T2 of the tumor compared to advanced T4 tumor. In contrast, the expression of inducible NOS was higher than in the advanced T4 tumor than in the earlier stages T2 of the tumor. The mapping of the expression of endothelial NOS, neuronal NOS and inducible NOS in human stomach showed higher expression of NOS isoforms in the distal third than in the proximal third of the stomach (P = 0.03, P = 0.04, P = 0.01, respectively). We conclude that there is greater expression of NOS in the stomach corpus and in antrum than in the proximal third of the normal human stomach mirroring the anatomical predilection of common pathological changes in this part of the human stomach. Furthermore, there was loss of the expression of individual isoenzymes in gastric neoplasms.      

Transoral application of EEA stapler after subtotal oesophagectomy.

OBJECTIVE: To describe a new transoral technique of cervical oesophagogastric and oesophagojejunal anastomoses using the EEA stapler. DESIGN: Prospective clinical study. SETTING: University Hospital, Bratislava, Slovakia. SUBJECTS: Two patients with squamous cell carcinoma of the middle and distal third of the oesophagus. INTERVENTIONS: Transhiatal subtotal oesophagectomy without thoracotomy, and cervical oesophageal anastomosis by transoral EEA stapling. MAIN OUTCOME MEASURES: Morbidity and mortality. RESULTS: Transoral stapling was successful in both patients with no anastomotic leaks. The patients were discharged on the 14th and 21st postoperative days, respectively. CONCLUSIONS: Transoral stapling of the cervical anastomosis gave good results in two patients. More development and evaluation are needed.     

Endoscopic Tri-Modal Imaging Improves Detection of Gastric Intestinal Metaplasia Among a High-Risk Patient Population in Singapore

Background

Detection of pre-neoplastic gastric mucosal changes and early gastric cancer (EGC) by white-light endoscopy (WLE) is often difficult. In this study we investigated whether combined autofluorescence imaging (AFI) and narrow band imaging (NBI) can improve detection of pre-neoplastic lesions and early gastric cancer in high-risk patients.

Patients and Methods

Chinese patients who were 50-years-old or above with dyspepsia were examined by both high-resolution WLE and combined AFI followed by NBI (AFI–NBI), consecutively in a prospective randomized cross-over setting, by two experienced endoscopists. The primary outcome was diagnostic ability of the two methods for patients with pre-neoplastic lesions such as intestinal metaplasia (IM) and mucosal atrophy.

Results

Sixty-five patients were recruited. One patient with large advanced gastric cancer was found and excluded from the analysis. Among the remaining 64 patients, 38 (59 %) had IM; of these, 26 (68 %) were correctly identified by AFI–NBI (sensitivity 68 %, specificity 23 %) and only 13 (34 %) by WLE (sensitivity 34 %, specificity 65 %). AFI–NBI detected more patients with IM than did WLE (p = 0.011). Thirty-one patients (48 %) had mucosal atrophy. Ten patients (32 %) were identified by AFI–NBI (sensitivity 32 %, specificity 79 %) and four patients (13 %) by WLE (sensitivity 13 %, specificity 88 %) (p = 0.100). No dysplasia or EGC was found.

Conclusion

AFI–NBI identified significantly more patients with IM than did WLE. Our result warrants further studies to define the role of combined AFI–NBI endoscopy for detection of precancerous conditions.     

RUNX3, a novel tumor suppressor, is frequently inactivated in gastric cancer by protein mislocalization

Loss of RUNX3 expression is suggested to be causally related to gastric cancer as 45% to 60% of gastric cancers do not express RUNX3 mainly due to hypermethylation of the RUNX3 promoter. Here, we examined for other defects in the properties of RUNX3 in gastric cancers that express RUNX3. Ninety-seven gastric cancer tumor specimens and 21 gastric cancer cell lines were examined by immunohistochemistry using novel anti-RUNX3 monoclonal antibodies. In normal gastric mucosa, RUNX3 was expressed most strongly in the nuclei of chief cells as well as in surface epithelial cells. In chief cells, a significant portion of the protein was also found in the cytoplasm. RUNX3 was not detectable in 43 of 97 (44%) cases of gastric cancers tested and a further 38% showed exclusive cytoplasmic localization, whereas only 18% showed nuclear localization. Evidence is presented suggesting that transforming growth factor-beta is an inducer of nuclear translocation of RUNX3, and RUNX3 in the cytoplasm of cancer cells is inactive as a tumor suppressor. RUNX3 was found to be inactive in 82% of gastric cancers through either gene silencing or protein mislocalization to the cytoplasm. In addition to the deregulation of mechanisms controlling gene expression, there would also seem to be at least one other mechanism controlling nuclear translocation of RUNX3 that is impaired frequently in gastric cancer.     

Fatal hepatitis B reactivation following discontinuation of nucleoside analogues for chronic hepatitis B

BACKGROUND: Nucleoside analogues such as lamivudine for chronic hepatitis B have an excellent safety profile while patients are on therapy but reactivation flares occur in 19-50% of patients after stopping therapy, some of whom develop liver decompensation. AIMS: To describe and report three cases who developed fatal hepatitis B reactivation after stopping nucleoside analogue therapy. SUBJECTS AND RESULTS: Three patients are described who developed hepatitis B reactivation and liver decompensation after stopping therapy. One of the three patients was participating in a famciclovir trial and the other two were receiving lamivudine therapy for active hepatitis B infection. All three patients had documented hepatitis B flares, and all had hepatitis B virus DNA detected at that time. All patients developed decompensated liver disease despite one patient having had a prior liver biopsy showing absence of cirrhosis. Reintroduction of lamivudine therapy failed to halt progression of liver decompensation even after hepatitis B virus DNA had been demonstrated to be absent. Sequencing for lamivudine resistant mutants in two cases where serum was available failed to show evidence of mutations associated with lamivudine resistance. CONCLUSION: Hepatitis B virus reactivation, leading to decompensation and death, are possible complications of treatment withdrawal and patients should be monitored closely if therapy is ceased.     

Expression of nitric oxide synthase, cyclooxygenase, and p53 in different stages of human gastric cancer

The present study evaluated the significance of nitric oxide synthase (NOS), cyclooxygenase (COX) expression and p53 status in 55 patients with gastric adenocarcinoma and relationship of these molecular markers to tumor characteristics and metastatic potential. Immunohistochemical technique was used to identify the cellular location and distribution of the enzymes in the specific cells of gastric tumors. In gastric cancer tissue, the expression of inducible enzymes, iNOS and COX-2, increased significantly with increasing tumor stage (P=0.015, P=0.001, respectively), size (P=0.025, P=0.001, respectively) and the presence of metastases (P=0.002, P=0.015, respectively). The expression of constitutive enzymes, ecNOS and COX-1, followed the opposite pattern. COX-1 was significantly reduced in advanced gastric tumors (P=0.007) and tumors larger than 5 cm (P=0.007). Reduced expression of ecNOS was also observed in advanced gastric tumors; however, this did not reach statistical significance. 53% of gastric tumors showed accumulation of p53. This was significantly higher in advanced tumors (P=0.004), larger than 5 cm (P=0.015) with metastases (P<0.001). Gastric tumors positive for accumulation of p53 had significantly stronger expression of iNOS (P=0.018) and COX-2 (P=0.01) enzymes than tumors negative for this nucleophosphoprotein. We conclude, that tumor-associated nitric oxide production, as well as COX-2 overexpression, may promote gastric cancer progression by providing a selective growth advantage to tumor cells with non-functioning p53.