(1/616) A case of advanced esophageal cancer showing a long-term complete response with chemotherapy with nedaplatin alone.
We describe a case of advanced esophageal cancer treated successfully by chemotherapy with nedaplatin alone. A 60-year-old male with type 2 advanced esophageal cancer, which was located in the upper part of the esophagus and had invaded adjacent organs, was treated with nedaplatin 150 mg/body (100 mg/m2) given intravenously every 4 weeks from January 6, 1991. He achieved a partial response (PR) and was discharged in March 1991. Subsequently, he received nedaplatin 75 mg/body in an out-patient setting almost every month until August 1992. Toxicities were tolerable and included mild thrombocytopenia and nausea/vomiting. From serial evaluation in October 1993, the esophageal tumor was not observed. After 7 years since initial chemotherapy was administered, he still survives without the disease. (+info)
(2/616) Oesophageal subepithelial fibrosis: an extension of oral submucosal fibrosis.
Fifty-five patients with oral submucosal fibrosis and an equal number of patients with no evidence of the disease were studied. All patients underwent upper gastrointestinal endoscopy and any abnormality was noted. Multiple oesophageal biopsies were obtained from the upper end of the oesophagus and from any endoscopically observed abnormality. The histological changes in the two groups were assessed blindly by an experienced histopathologist. Histological abnormalities were noted in the oesophageal mucosa in 2% of controls and 66% of patients with oral submucosal fibrosis (p < 0.0001). In the control group, acanthosis was seen in one patient, while in the patient group atrophy of the squamous epithelium was evident in 52%, hyperkeratosis in 52%, parakeratosis in 30%, dyskeratosis in 14%, acanthosis in 14%, and papillomatosis and mild dysplasia in 2% patients. Subepithelial collagenization was seen in 32 (64%) patients. The oesophageal abnormalities were seen more frequently in patients who had consumed Pan masala, Gutka, betel nut, tobacco or a combination of some or all of these, with or without betel leaf, for > or = 5 years compared to those consuming them for a shorter period of time (91% vs 46%, p < 0.001). It is concluded that oral submucosal fibrosis is not a disease confined to the oral cavity; the oesophagus may also be involved in about two-thirds of patients. (+info)
(3/616) Medication-induced oesophageal injury leading to broncho-oesophageal fistula.
Medication-induced oesophageal injury is one of the least recognised side-effects of oral medication and, in contrast to other oesophageal pathologies, is rarely considered in the differential diagnosis of chest pain. We describe a case of medication-induced oesophageal injury with a rare complication in which the diagnosis was not considered until the characteristic features were demonstrated at endoscopy. (+info)
(4/616) Omeprazole therapy decreases the need for dilatation of peptic oesophageal strictures.
BACKGROUND: Better control of gastric acid secretion with omeprazole appeared to decrease the need for dilatation of oesophageal strictures complicating gastro-oesophageal reflux disease in our hospital-based endoscopy service. AIM: To investigate whether the perceived decrease in the need for oesophageal dilatation could be documented from endoscopy records, and, if confirmed, whether this could be related to the treatment used. PATIENTS AND METHODS: Retrospective study of the records of 69 patients who had peptic oesophageal strictures dilated, followed by treatment with acid inhibition for at least 6 months. Mean duration of follow-up was 3.9 years during treatment with H2-receptor antagonists and 2.1 years while on omeprazole (258 and 78 patient-years, respectively). Re-dilatation rates were compared between those treated with H2-receptor antagonists or omeprazole. RESULTS: There has been a significant decrease in dilatations performed for gastro-oesophageal reflux induced strictures (P<0.001), while dilatation rates for other indications remained constant. Treatment with omeprazole not only decreased the need for further dilatations, but also prolonged the mean time between any further dilatations to 26.3 months compared to 9.3 months for those on an H2-receptor antagonist (P<0.0001). CONCLUSIONS: Following dilatation of peptic oesophageal strictures, treatment with omeprazole in place of an H2-blocker significantly decreases the need for repeat dilatation. (+info)
(5/616) Endoscopic regression of Barrett's oesophagus during omeprazole treatment; a randomised double blind study.
BACKGROUND: Barrett's oesophagus, columnar metaplasia of the epithelium, is a premalignant condition with a 50-100-fold increased risk of cancer. The condition is caused by chronic gastro-oesophageal reflux. Regression of metaplasia may decrease the cancer risk. AIMS: To determine whether elimination of acid gastro-oesophageal reflux induces a regression of metaplastic epithelium. METHODS: Sixty eight patients with acid reflux and proven Barrett's oesophagus were included in a prospective, randomised, double blind study with parallel groups, and were treated with profound acid secretion suppression with omeprazole 40 mg twice daily, or with mild acid secretion suppression with ranitidine 150 mg twice daily, for 24 months. Endoscopy was performed at 0, 3, 9, 15, and 24 months with measurement of length and surface area of Barrett's oesophagus; pH-metry was performed at 0 and 3 months. Per protocol analysis was performed on 26 patients treated with omeprazole, and 27 patients treated with ranitidine. RESULTS: Omeprazole reduced reflux to 0.1%, ranitidine to 9.4% per 24 hours. Symptoms were ameliorated in both groups. There was a small, but statistically significant regression of Barrett's oesophagus in the omeprazole group, both in length and in area. No change was observed in the ranitidine group. The difference between the regression in the omeprazole and ranitidine group was statistically significant for the area of Barrett's oesophagus (p=0. 02), and showed a trend in the same direction for the length of Barrett's oesophagus (p=0.06). CONCLUSIONS: Profound suppression of acid secretion, leading to elimination of acid reflux, induces partial regression of Barrett's oesophagus. (+info)
(6/616) Maintenance therapy with pantoprazole 20 mg prevents relapse of reflux oesophagitis.
BACKGROUND: Proton pump inhibitors can be effective as maintenance therapy in reducing the relapse rate of reflux oesophagitis at a dose lower than that used for acute healing. PATIENTS AND METHODS: Patients (n=396, 18-88 years old) with healed reflux oesophagitis (grade II or III before healing) were included in this multinational, prospective, parallel-group, randomized double-blind study. They took oral pantoprazole 20 mg (n=203) or 40 mg (n=193), once daily for up to 12 months. Scheduled endoscopies were performed at entry, after 6 and 12 months, or when symptoms of at least moderate intensity were perceived on 3 consecutive days; symptoms were assessed every 3 months. The primary efficacy parameter was the time until endoscopically proven relapse of reflux oesophagitis occurred; the secondary parameters included tolerability, safety and time until symptomatic relapse occurred. RESULTS: Analysis was performed using the 'all-patients-treated' approach. Endoscopic relapse rates in the 20 mg group after 6 and 12 months were 16 and 29%, respectively; in the 40 mg group, they were 7 and 19%, respectively. Symptomatic relapse rates after 6 and 12 months were 14 and 21% in the 20 mg group and 10 and 17% in the 40 mg group, respectively. Pantoprazole 20 mg and 40 mg were well tolerated throughout the study; the type and frequency of adverse events reported were similar for both treatment groups. CONCLUSION: The 20 mg dose was proven to be 'at least equivalent' to the 40 mg dose with respect to endoscopic and symptomatic relapse. The 20 mg once daily dose represents an effective and safe maintenance regimen for the majority of patients with healed reflux oesophagitis. (+info)
(7/616) Endoscopic evaluation of gastro-esophageal reflux disease.
Endoscopy is, currently, the initial investigation of choice for the investigation of gastroesophageal reflux disease (GERD) in clinical practice and clinical research. Erosion severity is predictive of a patient's response to therapy and of the likelihood of relapse after therapy. It is, therefore, important to grade the severity of erosive reflux esophagitis, particularly in the context of clinical trials. The Savary-Miller endoscopic classification system is used widely but usage and interpretation are very variable. The "MUSE" (metaplasia [M], ulceration [U], stricturing [S] and erosions [E]) classification provides clear definitions of the relevant endoscopic features, and it is based on a standardized report form, which allows the endoscopist to make a clear record of esophagitis severity. Recent studies confirm that endoscopists can identify erosions or mucosal breaks, ulcers, strictures, and metaplasia reproducibly. The "L.A." (Los Angeles) classification describes four grades of esophagitis severity (A to D), based on the extent of esophageal lesions known as "mucosal breaks," but it does not record the presence or severity of other GERD lesions. Thus, for patients with "complicated" reflux disease, the "MUSE" classification offers a more comprehensive description of esophagitis severity. Endoscopy is not universally applicable: 40 to 60 percent of patients with typical reflux symptoms do not have esophageal erosions and are now considered to have "endoscopy negative reflux disease" (ENRD). Thus, endoscopy is not the final arbiter as to a diagnosis of reflux disease, and it is not, therefore, a necessary prerequisite to therapy. Endoscopy is indicated at first presentation for patients with alarm symptoms referable to the upper gastrointestinal tract. It has also been proposed that all patients with chronic GERD should have a "once-in-a-lifetime" endoscopy; in the absence of Barrett's esophagus or other complications, no follow-up is required unless the patient's symptoms change significantly. A surveillance program with multiple biopsies should be instituted if there is evidence of Barrett's esophagus. Endoscopic evaluation should document the presence and extent of esophageal erosions using the L.A. or MUSE classification systems; complications should also be documented and may be recorded using the MUSE classification. Non-erosive changes such as erythema may be ignored on the basis of present evidence, and there are no clear data to support the use of endoscopic biopsies for the diagnosis of GERD. (+info)
(8/616) Management of gastroesophageal reflux disease: the primary care strategy.
Gastroesophageal reflux disease (GERD) is a common problem in the community and in general practice. General practitioners and family physicians need to understand patients' reasons for consultation and also be aware of alarm symptoms suggestive of serious disease. A primary care management strategy for GERD is proposed, in which the place of endoscopic and other investigations is defined, the role of lifestyle modification discussed, and recommendations for longer-term therapy and management are made. (+info)