Michalis Tzivras

Jejunogastric intussusception presented with hematemesis: a case presentation and review of the literature

BackgroundJejunogastric intussusception (JGI) is a rare but potentially very serious complication of gastrectomy or gastrojejunostomy. To avoid mortality early diagnosis and prompt surgical intervention is mandatory.Case presentationA young man presented with epigastric pain and bilous vomiting followed by hematemesis,10 years after vagotomy and gastrojejunostomy for a bleeding duodenal ulcer. Emergency endoscopy showed JGI and the CT scan of the abdomen was compatible with this diagnosis. At laparotomy a retrograde type II, JGI was confirmed and managed by reduction of JGI without intestinal resection. Postoperative recovery was uneventful.ConclusionsJGI is a rare condition and less than 200 cases have been published since its first description in 1914. The clinical picture is almost diagnostic. Endoscopy performed by someone familiar with this rare entity is certainly diagnostic and CT-Scan of the abdomen could also help. There is no medical treatment for acute JGI and the correct treatment is surgical intervention as soon as possible.

Expression of HLA-DR, costimulatory molecules B7-1, B7-2, intercellular adhesion molecule-1 (ICAM-1) and Fas ligand (FasL) on gastric epithelial cells in Helicobacter pylori gastritis; influence of H. pylori eradication

There is evidence that Helicobacter pylori infection up‐regulates the expression of HLA class II molecules by gastric epithelial cells (GEC). In this study we evaluated whether GEC are capable of expression of costimulatory molecules in H. pylori gastritis. The expression of FasL by GEC, before and after eradication of H. pylori, was also studied. Thirty patients (23 men) aged 27–81 years (53·67 ± 13·99 years (mean ± s.d.)) with dyspepsia were studied. Upper gastrointestinal endoscopy was performed and six biopsies were obtained (antrum, n= 3; corpus, n= 3) for Campylobacter‐Like Organisms (CLO) test and histology; 23 (16 men) were H. pylori+ and seven (all men) were H. pylori− by both methods and served as controls. Helicobacter pylori eradication therapy was given to H. pylori+ patients and all patients were re‐endoscoped after 116 ± 9 days. Formalin‐fixed paraffin‐embedded tissue sections were stained by the ABC immunoalkaline phosphatase method. In H. pylori gastritis HLA‐DR was expressed and correlated with disease activity (P < 0·01). No HLA‐DR was observed in controls. In H. pylori‐eradicated patients significant decrease of HLA‐DR was found (antrum, P < 0·001). ICAM‐1 was expressed by GEC in 80% of H. pylori+ patients; ICAM‐1 expression did not correlate with gastritis parameters and decreased significantly after eradication (antrum, P < 0·01). B7‐1 and B7‐2 were expressed on H. pylori+ samples and their expression decreased after eradication, albeit not significantly. Weak epithelial expression of both B7 molecules was observed in all the controls. FasL was steadily expressed by GEC in both H. pylori+ and H. pylori− patients and remained almost unchanged after eradication. These findings suggest that GEC may acquire antigen‐presenting cell properties in H. pylori infection through de novo expression of HLA‐DR and costimulatory molecules. This seems to be attenuated after eradication and resolution of mucosal inflammation. The same cells exhibit the capacity to control the inflammatory process, probably by inducing apoptotic cell death to Fas‐bearing infiltrating lymphocytes.

Alterations in the Proliferating Compartment of Gastric Mucosa during Helicobacter Pylori Infection: The Putative Role of Epithelial Cells Expressing p27kip1

The proliferating zone contains stem cells that give rise to all epithelial cells of the gastric mucosa. In the present study, we investigated the turnover of gastric epithelial cells in the proliferating zone of Helicobacter pylori–infected mucosa, with or without intestinal metaplasia, before and after eradication of the microorganism. In addition, we studied the topographical distribution of the cyclin dependent kinase inhibitor p27Kip1, which plays a critical role in cell cycle progression and differentiation programs. Twenty-eight patients (22 male), aged 32–78 years and with dyspeptic symptoms, were endoscoped, and gastric biopsies were obtained from antrum and corpus for histopathological examination and the Campylobacter-like organisms test; eradication therapy was given to infected patients, and all patients were re-endoscoped after 105 ± 33 days (mean ± SD). The kinetics of gastric epithelial cells and p27Kip1 status was assessed by means of immunohistochemistry and TUNEL (Tdt-mediated dUTP-biotin nick end labeling) assay. Twenty-one (21) of 28 patients were H. pylori positive, and 7 were found H. pylori negative and served as controls. In antrum, intestinal metaplasia was detected in 7/21 (33.3%). In H. pylori gastritis, Ki67 expression was found increased in the proliferating zone, compared with normal (P = .03); analogous results were obtained with the other proliferation markers, namely retinoblastoma protein and topoisomerase IIα. An inverse relationship between proliferation index and atrophy was disclosed (P = .02). A reduction in the proliferation index was observed after eradication, albeit not significant. Apoptotic epithelial cells were found significantly increased (P < .01) in H. pylori gastritis, and a significant reduction was observed after eradication (P < .01). In addition, apoptotic index was found to correlate with H. pylori density. The topographical study of p27Kip1 revealed a p27kip1-positive epithelial cell population that resided deep in the proliferating zone; these cells were considered to be stem cells and were found significantly increased in areas with intestinal metaplasia (P < .05); in H. pylori gastritis, there was also an increase that did not reach statistical significance. H. pylori infection induces apoptosis and increases proliferation in the proliferating zone. The increased cellular turnover, together with the increased number of putative p27Kip1-positive stem cells in the context of intestinal metaplasia, provides further evidence for the role of H. pylori infection in gastric carcinogenesis.

Changes in Adaptive and Innate Immunity in Patients with Acute Pancreatitis and Systemic Inflammatory Response Syndrome

Background: Acute pancreatitis is a form of inflammation with clinical features ranging from pancreatic inflammation to fatal systemic manifestations. The aim of this study was to clarify changes in lymphocyte subsets and alterations in the functioning of natural killer (NK) cells. Patients and Methods: Forty-five patients were enrolled into the study; 35 with acute pancreatitis and systemic inflammatory response syndrome (SIRS) and 10 healthy subjects. Blood was sampled early from all patients. Blood immune cells were studied on days 1 and 4 by flow cytometry. Tumor necrosis factor-α (TNFα) and interleukin (IL)-6 were estimated from supernatants of NK cells before/after stimulation with lipopolysaccharide (LPS). Results: Apoptosis in patients was significantly different on days 1 and 4 compared with controls. Apoptosis of CD4(+) lymphocytes was significantly correlated with the days to resolution of SIRS (r = +0.586, p = 0.022). Significant differences were observed in TNFα and IL-6 on day 1 with/without LPS stimulation between patients and healthy individuals. Significantly increased levels of TNFα and IL-6 were found after LPS stimulation compared with unstimulated supernatants in day 1. Conclusion: NK cells altered their secretory status when stimulated with LPS. This finding could be explained by the cellular reprogramming of NK cells in the field of acute pancreatitis and SIRS.

Implications for a role of interleukin‐23 in the pathogenesis of chronic gastritis and of peptic ulcer disease

The present study aimed to investigate the role of gastric mucosa for the secretion of interleukin (IL)‐23 in chronic gastritis. One hundred and one patients were enrolled; 47 with duodenal ulcer, 33 with gastric ulcer and 31 with chronic gastritis. Biopsies were incubated in the absence/presence of endotoxins. Supernatants were collected and IL‐23 and IL‐1β were measured by enzyme‐linked immunosorbent assay. Scoring of gastritis was performed according to the updated Sydney score. Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis. IL‐23 was higher in supernatants of tissue samples of Helicobacter pylori‐positive than of H. pylori‐negative patients. No differences were recorded in concentrations of IL‐23 and IL‐1β between patients with duodenal ulcer, gastric ulcer and chronic gastritis. Positive correlations were found between IL‐23 of patients with both duodenal and gastric ulcer and chronic gastritis and the degree of infiltration of neutrophils and monocytes. Similar correlations were observed between IL‐23 and IL‐1β. IL‐23 secreted by the gastric mucosa could be implicated in the pathogenesis of chronic gastritis. IL‐23 was released in the presence of H. pylori from the inflamed gastric mucosa and followed the kinetics of IL‐1β.

Lipid peroxidation in chronic gastritis; any influence of Helicobacter pylori?

In an attempt to investigate the significance of lipid peroxidation in the pathogenesis of gastritis associated with or without Helicobacter pylori infection, malonodialdehyde (MDA) levels were measured by the thiobarbiturate assay in the gastric juice of 101 patients undergoing upper GI endoscopy and correlated with histopathological findings. Elevated MDA levels were found in all patients with gastritis compared with controls. MDA levels were significantly correlated with the extent of the mucosal inflammation and with disease activity in patients with reactive gastritis. In patients with H. pylori associated gastritis MDA levels were not correlated with disease activity but rather with the degree of atrophy. In this case, MDA levels were equal or even less than in patients with reactive gastritis. MDA levels were not affected by the history of consumption of PPIs, of H(2)-blockers or of NSAIDs over the last month before the endoscopy. It is concluded that lipid peroxidation is a mechanism involved in the pathogenesis of gastritis associated or not to H. pylori infection.

High eradication rate of Helicobacter pylori using a four-drug regimen in patients previously treated unsuccessfully

The objective of this study was to assess the efficacy of a new regimen in eradicating Helicobacter pylori (Hp) in patients with duodenal ulcer (DU) who were previously treated unsuccessfully with standard triple therapy (tripotassium dicitratobismuthate [TDB] 120 mg QID, metronidazole 500 mg TID, and tetracycline 500 mg QID) or proton-pump inhibitor (PPI) dual therapy (omeprazole 20 mg BID and amoxicillin 500 mg QID). The study included 133 consecutive patients aged 17 to 83 years with endoscopically diagnosed DU (diameter > or = 5 mm) in whom standard triple therapy or PPI dual therapy had failed to eradicate Hp. A rapid urease (CLO) test was performed on four biopsy specimens at study entry and at least 1 month after the end of treatment to confirm Hp colonization and eradication, respectively. Patients were considered to be Hp positive if any CLO test was positive within 2 hours, and Hp was considered to be eradicated if all CLO tests were still negative after 24 hours. In 31 randomly selected patients, Hp eradication was confirmed histologically as well. Patients were given omeprazole 60 mg/d (20 mg in the morning and 40 mg in the evening) plus amoxicillin 500 mg QID for 10 days and subsequently were given metronidazole 500 mg TID for 10 days plus TDB 120 mg QID for 6 weeks. One hundred and twenty-four patients were followed up; five (4%) withdrew because of side effects (protracted diarrhea, stomatitis, skin rashes). Per-protocol analysis showed Hp eradication in 113 of 119 patients (95%) and ulcer healing in 118 of 119 (99%). Intent-to-treat analysis showed an Hp eradication rate of 85% (113 of 133 patients) and an ulcer healing rate of 89% (118 of 133 patients). In per-therapy analysis, the Hp eradication rate was 91% (113 of 124 patients), and the ulcer healing rate was 95% (118 of 124 patients). Side effects were observed in 39 of 119 patients (33%) and were generally mild. The four-drug regimen used in this study, when given to patients previously treated unsuccessfully with standard triple therapy or PPI dual therapy, was highly effective in eradicating Hp and healing DUs and had no major side effects.

Diagnosis of Helicobacter pylori infection with a stool assay: is it useful after eradication treatment?

In two of these studies, the use of tamoxifen with a dosage of #30 mg/day has been shown to result in favorable survival outcome. Although the comment on the short survival (median 5 44 days) of our patients with tamoxifen treatment was valid, none of the 27 patients who survived more than 3 months had partial response to tamoxifen treatment. As mentioned in the Results section of the article, analysis of the survival results after retrospective exclusion of the patients with short survival did not show any beneficial effect of tamoxifen treatment. These might suggest that even when serum therapeutic level of tamoxifen was achieved in patients with adequate survival, it did not result in survival benefit. Chi-Leung Liu, M.S., F.R.C.S. (Edin) Irene Oi-Lin Ng, M.D., F.R.C.Path. (UK) Sheung-Tat Fan, M.S., M.D., F.R.C.S. (Glasg & Edin) Centre of Liver Diseases and Departments of Surgery and Pathology University of Hong Kong Medical Centre Queen Mary Hospital Hong Kong, China

Ranitidine Versus Ranitidine plus Octreotide in the Treatment of Acute Non-variceal Upper Gastrointestinal Bleeding: A Prospective Randomised Study

Summary Aim: To compare the efficacy of ranitidine with that of ranitidine plus octreotide in the treatment of non-variceal upper gastrointestinal (UGI) bleeding. Design: Prospective, randomised, open study. Patients and Methods: Upper GI endoscopy was carried out during the first 24 hours in all patients with UGI bleeding who had been admitted within a period of 18 months. Patients with variceal bleeding, and those who had undergone any type of gastric operation, were excluded. Eighty-four patients (58 men and 26 women) aged 21–92 years (mean age: 61.2 ± 15.0 SD) were included. Patients were randomised to receive ranitidine 50 mg tid intravenously alone (Group A: 44 patients, 29 men), or in combination with octreotide 100 µg tid subcutaneously, the second drug given for three days only (Group B: 40 patients, 29 men). The study end-points were discharge without operation, emergency surgical intervention or death. The number of blood units given and the days of hospitalisation were also recorded. Results: Aspirin and non-aspirin NSAID use before bleeding was reported by 16/44 (36%) patients in Group A and by 19/40 (47.5%) patients in Group B (p = 0.38, OR = 0.63, 95% CI = 0.26–1.51). The endoscopically detected pathology and bleeding stigmata did not differ between the groups (p = 0.86, p = 0.64, OR = 0.78, 95% CI = 0.3–1.99, respectively). Mean use of blood units (p = 0.16) and days of hospitalisation (p = 0.25) did not differ. Three patients in Group A (6.8%) and three in Group B (7.5%) required surgical intervention (p = 1.0, OR = 1.1, 95% CI = 0.21–5.84). Conclusion: Ranitidine plus subcutaneous octreotide is not superior to ranitidine alone in the management of patients with acute non-variceal UGI bleeding.

Diffuse malignant peritoneal mesothelioma presenting as intestinal obstruction.

Diffuse malignant peritoneal mesothelioma (DMPM) represents 90% of all peritoneal forms of mesothelioma. It affects mainly patients 50-69 years old. In 50% of cases there is a history of asbestos exposure. The clinical presentation of the disease is not characteristic: nonspecific abdominal pain, weight loss, and abdominal distension are common. Ascites occurs in 90% of the patients. Bowel obstruction is a late manifestation. We present three patients with DMPM, without a history of asbestos exposure and without ascites, who presented with complete bowel obstruction. All patients underwent emergency operations, and palliative surgical procedures were performed. Each patient died within 3 to 6 months postoperatively.