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5.
J Gastroenterol ; 51(2): 104-11, 2016 Feb.
Article in English | MEDLINE | ID: mdl-25940151

ABSTRACT

BACKGROUND: Whether proton pump inhibitors (PPIs) relieve heartburn or precordial pain after endoscopic resection (ER) for esophageal squamous cell carcinoma (ESCC) remains unclear. The aim of this study was to investigate the efficacy of PPI therapy for these symptoms after ER for ESCC. METHODS: We conducted a multicenter prospective randomized controlled trial among 15 hospitals in Japan. In total, 229 patients with cT1a ESCC were randomly assigned to receive PPI therapy for 5 weeks after ER (the PPI group, n = 115) or follow-up without PPI therapy (the non-PPI group, n = 114). The primary end point was the incidence of gastroesophageal reflux disease (GERD)-like symptoms after ER from a self-reported questionnaire (Frequency Scale for Symptoms of GERD). Secondary end points were ulcer healing rate at 5 weeks, incidence of pain, improvement rate of symptoms in those who started PPI therapy because of GERD-like symptoms in the non-PPI group, and adverse events. RESULTS: No significant difference was observed in the incidence of GERD-like symptoms after ER between the non-PPI and PPI groups (30 % vs 34 %, respectively). No significant differences were observed in the ulcer healing rate at 5 weeks (84 % vs 85 %) and incidence of pain within 1 week (36 % vs 45 %). In nine of ten patients (90 %) who started PPI therapy because of GERD-like symptoms in the non-PPI group, PPI administration relieved GERD-like symptoms. No adverse events related to PPI administration were observed. CONCLUSION: PPI therapy is not efficacious in reducing symptoms and did not promote healing of ulcers in patients undergoing ER for ESCC.


Subject(s)
Carcinoma, Squamous Cell/surgery , Esophageal Neoplasms/surgery , Esophagoscopy/adverse effects , Gastroesophageal Reflux/drug therapy , Proton Pump Inhibitors/therapeutic use , Adult , Aged , Carcinoma, Squamous Cell/pathology , Esophageal Diseases/drug therapy , Esophageal Diseases/etiology , Esophageal Neoplasms/pathology , Esophageal Squamous Cell Carcinoma , Esophagoscopy/methods , Female , Gastroesophageal Reflux/etiology , Heartburn/drug therapy , Heartburn/etiology , Humans , Male , Middle Aged , Pain Measurement/methods , Pain, Postoperative/drug therapy , Pain, Postoperative/etiology , Prospective Studies , Severity of Illness Index , Treatment Outcome , Ulcer/drug therapy , Ulcer/etiology
9.
Ann Oncol ; 20(8): 1397-401, 2009 Aug.
Article in English | MEDLINE | ID: mdl-19457938

ABSTRACT

BACKGROUND: Smoking may affect the efficacy of chemotherapy and the incidence of adverse events. We investigated the correlation between smoking history and gemcitabine-induced neutropenia. PATIENTS AND METHODS: Data on smoking history and incidence of grade 3-4 neutropenia were retrospectively gathered for 103 chemo-naive patients treated with gemcitabine monotherapy (59 patients with pancreatic, 41 with hepatobiliary and three with other cancers). RESULTS: There was a significantly higher incidence of grade 3-4 neutropenia among patients without a history of smoking (55.7%) than among those with a history of smoking (including current and ex-smokers; 23.6%) [odds ratio (OR) 0.244, 95% confidence interval (CI) 0.105-0.569; P < 0.001]. After adjustment for age, gender, platelet and baseline neutrophil counts, history of surgery for primary cancer, creatinine concentration, hemoglobin concentration, aspartate aminotransferase concentration, alanine aminotransferase concentration and total bilirubin concentration, logistic regression analysis identified a history of smoking as an independent inverse predictor of gemcitabine-induced neutropenia (OR 0.188, 95% CI 0.057-0.618; P = 0.006). CONCLUSION: Patients without a history of smoking may be at higher risk of developing gemcitabine-induced neutropenia. The mechanism underlying this phenomenon is unclear at this point.


Subject(s)
Antimetabolites, Antineoplastic/adverse effects , Deoxycytidine/analogs & derivatives , Neutropenia/chemically induced , Neutropenia/metabolism , Smoking/metabolism , Adult , Aged , Aged, 80 and over , Antimetabolites, Antineoplastic/administration & dosage , Antimetabolites, Antineoplastic/pharmacokinetics , Biliary Tract Neoplasms/blood , Biliary Tract Neoplasms/drug therapy , Deoxycytidine/administration & dosage , Deoxycytidine/adverse effects , Deoxycytidine/pharmacokinetics , Female , Humans , Liver Neoplasms/blood , Liver Neoplasms/drug therapy , Male , Middle Aged , Pancreatic Neoplasms/blood , Pancreatic Neoplasms/drug therapy , Retrospective Studies , Smoking/adverse effects , Gemcitabine
10.
Oncogene ; 26(40): 5927-38, 2007 Aug 30.
Article in English | MEDLINE | ID: mdl-17384682

ABSTRACT

Radiotherapy is an effective treatment for some esophageal cancers, but the molecular mechanisms of radiosensitivity remain unknown. RUNX3, a novel tumor suppressor of gastric cancer, functions in transforming growth factor (TGF)-beta-dependent apoptosis. We obtained paired samples from 62 patients with advanced esophageal cancers diagnosed initially as T3 or T4 with image diagnosis; one sample was obtained from a biopsy before presurgical radiotherapy, and the other was resected in surgical specimens after radiotherapy. RUNX3 was repressed in 67.7% cases of the pretreatment biopsy samples and 96.7% cases of the irradiated, resected samples. The nuclear expression of RUNX3 was associated with radiosensitivity and a better prognosis than cytoplasmic or no RUNX3 expression (P<0.003); cytoplasmic RUNX3 expression was strictly associated with radioresistance. RUNX3 was downregulated and its promoter was hypermethylated in all radioresistant esophageal cancer cell lines examined. Stable transfection of esophageal cancer cells with RUNX3 slightly inhibited cell proliferation in vitro, enhanced the antiproliferative and apoptotic effects of TGF-beta and increased radiosensitivity in conjunction with Bim induction. In contrast, transfection of RUNX3-expressing cells with a RUNX3 antisense construct or a Bim-specific small interfering RNA induced radioresistance. Treatment with 5-aza-2'-deoxycytidine restored RUNX3 expression, increased radiosensitivity and induced Bim in both control and radioresistant cells. These results suggest that RUNX3 silencing promotes radioresistance in esophageal cancers. Examination of RUNX3 expression in pretreatment specimens may predict radiosensitivity, and induction of RUNX3 expression may increase tumor radiosensitivity.


Subject(s)
Carcinoma, Squamous Cell/genetics , Carcinoma, Squamous Cell/radiotherapy , Core Binding Factor Alpha 3 Subunit/genetics , Esophageal Neoplasms/genetics , Esophageal Neoplasms/radiotherapy , Gene Expression Regulation, Neoplastic , Gene Silencing , Aged , Biopsy , Carcinoma, Squamous Cell/diagnosis , Cell Differentiation , Cell Nucleus/metabolism , Esophageal Neoplasms/diagnosis , Female , Humans , Male , Middle Aged , Prognosis , Radiation Tolerance
12.
Abdom Imaging ; 32(3): 348-50, 2007.
Article in English | MEDLINE | ID: mdl-16897276

ABSTRACT

We report a unique case of acute cholecystitis due to strangulation of a floating gallbladder by the lesser omentum, which could be detected by abdominal ultrasonography. We believe this case to be the first case of reported literatures in English.


Subject(s)
Cholecystitis, Acute/etiology , Gallbladder/abnormalities , Adult , Bromhexine , Cholecystitis, Acute/diagnostic imaging , Cholecystography , Female , Humans , Omentum , Torsion Abnormality , Ultrasonography
17.
Gut ; 51(5): 742-5, 2002 Nov.
Article in English | MEDLINE | ID: mdl-12377817

ABSTRACT

The prevalence of Helicobacter pylori infection is very low in patients with fundic gland polyps (FGPs) of the stomach. We report here two cases with multiple FGPs that regressed following new H pylori acquisition. Patient Nos I and II had multiple FGPs in normal fundic mucosa without inflammatory changes or atrophy. Both were not infected with H pylori. Following acquisition of H pylori infection however, all FGPs in both patients completely disappeared except for one FGP in patient No I. Although the size of the remaining polyp in patient No I was greatly reduced after H pylori acquisition, it became enlarged again after eradication. Interestingly, in the remaining polyp, we found an activating beta-catenin gene mutation whereas no such mutations were detected in FGPs of patient No II. Thus H pylori infection may have an inhibitory effect on the development of FGPs.


Subject(s)
Gastritis/microbiology , Helicobacter Infections , Helicobacter pylori , Neoplasm Regression, Spontaneous , Polyps/microbiology , Stomach Neoplasms/microbiology , Adult , Aged , Cytoskeletal Proteins/genetics , DNA Mutational Analysis , Female , Gastric Fundus , Gastritis/pathology , Helicobacter Infections/pathology , Humans , Male , Neoplasm Proteins/genetics , Neoplasm Regression, Spontaneous/genetics , Polymerase Chain Reaction , Polyps/genetics , Polyps/pathology , Stomach Neoplasms/genetics , Stomach Neoplasms/pathology , Trans-Activators/genetics , beta Catenin
18.
Endoscopy ; 34(4): 343-6, 2002 Apr.
Article in English | MEDLINE | ID: mdl-11932795

ABSTRACT

It remains unclear whether lymphoma of the mucosa-associated lymphoid tissue (MALT) in the extragastric organs is related to Helicobacter pylori infection or not. This report describes three patients with rectal MALT lymphoma negative for H. pylori infection, all of whom showed disease regression after being treated with antibiotics. One patient had MALT lymphoma in both the descending colon and the rectum; the other two patients had rectal disease only. None of the patients had chronic gastritis which was detectable either endoscopically or histologically and H. pylori infection was completely ruled out by various methods, including a urease breath test. These patients received antibiotic therapy. In all the patients, regression of MALT lymphoma was observed endoscopically and histologically, and polymerase chain reaction revealed that a previously observed rearranged band of immunoglobulin heavy chain had also disappeared after antibiotic treatment. These cases therefore suggest involvement of micro-organisms other than H. pylori in the development of rectal MALT lymphoma.


Subject(s)
Helicobacter Infections/diagnosis , Helicobacter pylori/isolation & purification , Intestinal Mucosa/pathology , Lymphoma, B-Cell, Marginal Zone/pathology , Rectal Neoplasms/pathology , Adult , Aged , Anti-Bacterial Agents , Biopsy, Needle , Colonoscopy , Drug Therapy, Combination/administration & dosage , Female , Follow-Up Studies , Helicobacter Infections/drug therapy , Helicobacter pylori/drug effects , Humans , Lymphoma, B-Cell, Marginal Zone/microbiology , Middle Aged , Rectal Neoplasms/microbiology , Risk Assessment , Tomography, X-Ray Computed , Treatment Outcome
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