Empirical H2 blocker therapy or prompt endoscopy in the management of dyspepsia.
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Biomedical subjects
Publications and source records attributed to M B Fennerty.
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OBJECTIVE: to determine whether balloon cytology would allow a nonendoscopic diagnosis of Barrett's esophagus. METHODS: In 10 unselected patients with Barrett's esophagus, balloon cytology was performed with a Brandt esophageal cytology balloon catheter prior to endoscopy/esophageal biopsy. Specimens were cytologically evaluated for the presence of goblet cells and/or dysplasia. RESULTS: No patient had goblet cells or definitive columnar cell dysplasia. CONCLUSION: This technique with a commercially available balloon catheter does not allow for a nonendoscopic diagnosis of Barrett's esophagus.
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Helicobacter pylori is the cause of chronic active gastritis. It is integral to the pathogenesis of peptic ulcer disease and is epidemiologically linked to gastric cancer and lymphoma. Helicobacter pylori can be detected through a variety of invasive (urease testing, culture, or histologic diagnosis of endoscopic biopsies) and noninvasive (urease breath tests, serologic tests) diagnostic tests. It is now appropriate to detect and eradicate H pylori in patients with a peptic ulcer as the natural history of peptic ulcer disease is then markedly improved. At this time, there is no role for H pylori eradication in the prevention of gastric cancer; however, this concept is being actively investigated. There is no indication to treat patients who have H pylori and nonulcer dyspepsia or gastritis because eradication does not reliably affect their symptoms. Current regimens for eradication include bismuth, antibiotics, and antisecretory agents. Complex and poorly tolerated regimens (triple therapy) may no longer be necessary, as simpler regimens (omeprazole and amoxicillin or clarithromycin) appear to be as effective and better tolerated.
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Patients with chronic atrophic gastritis intestinal metaplasia (IM) are suspected of being at increased risk for the intestinal type of gastric cancer. Diet is one of several etiologic components that may contribute to the development of the IM lesion. One hundred patients (50 with IM and 50 without IM) were evaluated to determine their dietary intake of nitrosating agents and vitamin C and their smoking habits. Patients with IM reported a higher consumption of two foods rich in nitrosating agents, bacon (.28 vs. .10, p = .02) and sausages (.16 vs. .02, p = .01), compared to patients without IM. Smoking and vitamin C intake were similar in both the IM-positive and the IM-negative groups.
Tissue staining has broad clinical and research application in gastroenterology but remains underused. New application and the development of novel "stains" should result in improved detection of gastrointestinal disease. Expanded research in tissue staining is needed and data on outcome effectiveness awaited.
OBJECTIVES: The prevalence of colon polyps increases with age in the general population. It is unknown whether a lack of adenomatous polyps determined at one time point after the age of 50 is predictive of a subsequent low risk of polyp development. METHODS: Twenty-nine patients between ages 50 and 70 who had no prior history of polyps and had a normal colonoscopy at least 5 yr previously were recruited for follow-up colonoscopy to evaluate the incidence of neoplastic disease in this presumably low-risk group. RESULTS: The incidence of adenomatous polyps after a mean of 5.74 yr was 41.4% (95% confidence interval: 23.5-61.1%). A total of 20 adenomatous polyps were found in 12 patients. Seven polyps were 5 mm or more in size. CONCLUSIONS: We conclude that in patients with no history of colonic neoplasia who are 50 yr old, or older, the finding of a normal colonoscopy does not predict diminished risk of neoplasia.
OBJECTIVES: We attempted to determine an accurate frequency of new polyp growth in a cohort of veteran male patients who were initially cleared of polyps by tandem colonoscopy. METHODS: Followup colonoscopy was performed 2 yr after tandem colonoscopy. A polyp was categorized as "new" if it was not located in a segment of the colon or rectum that had harbored a neoplastic polyp of the same histology at tandem colonoscopy, in contradistinction to lesions designated as "same-segment" polyps. RESULTS: Fifty-eight of 90 patients who had tandem colonoscopy as a part of a previous study were available for follow-up colonoscopy for 2 yr. Ninety-one percent had a history of benign neoplastic polyps or cancer. Neoplastic polyps were documented in 52% (95% CI, 45-74%) of patients at followup, and 38% (95% CI, 26-52%) were found to have a total of 31 "new" lesions. All new lesions were tubular adenomas. The largest number of new polyps in an individual patient was four, and the largest new lesion was 20 mm in size with a flat, linear configuration. Most (25/31) new polyps were < or = 5 mm, and the number of neoplastic polyps per patient at follow-up was less than at tandem colonoscopy. CONCLUSIONS: Approximately one-half of older, male patients with a history of neoplastic polyps will demonstrate neoplastic polyps at 2 yr. In at least one-third of patients, these appear to be new lesions. In some patients, de novo neoplastic polyps can grow to > or = 1 cm within 2 yr.
OBJECTIVE: To determine the safety and efficacy of endoscopic balloon dilation for ulcer-induced gastric outlet strictures. METHODS: Review of the cumulative experience from two institutions involving 30 patients who underwent endoscopic balloon dilation for peptic ulcer-induced gastric outlet obstruction. Follow-up was by standardized interview at a mean of 15 months (range 4-28 months). RESULTS: Symptoms occurred for an average of 6 months before dilation and included weight loss, epigastric pain, nausea, vomiting, early satiety, bloating, and anorexia. Gastric outlet strictures had a median diameter of 6 mm (range, 0-10 mm). Ten (33%) patients had active ulcers. Six-millimeter to 18-mm (median 15-mm) balloons were inflated a median of 2 times (range 1-4 times) for a median of 60 s (range 30-180 s). Fifty-one procedures (1.7/patient) were performed; 20 (67%) patients had one treatment and 10 (33%) had multiple treatments. Twenty-four (80%) patients achieved sustained symptom relief, 17 of 20 having a single procedure and 7 of 10 required multiple sessions. Dilation failed in 4 (13%) patients with long duodenal strictures. Two (6.7%) patients dilated to 18 mm suffered perforation. Both recovered uneventfully after surgery. CONCLUSIONS: Endoscopic balloon dilation is safe and effective for most patients with ulcer-induced gastric outlet obstruction.
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Although a great deal of investigation has led to some novel approaches in treating primary sclerosing cholangitis (PSC) and primary biliary cirrhosis (PBC), no method has been proven to definitively alter the long-term outcome of either disease. In addition, many of the medical regimens reviewed in this article have serious toxicity, which limits their widespread use. Furthermore, the natural history of PSC and PBC may vary widely between individual patients, complicating the decision of whom and when to treat. Ursodeoxycholic acid (Actigall) appears to be a safe and possibly effective agent for both diseases in their early stages, and its use in selected patients may be warranted. Methotrexate (Folex, Mexate, Rheumatrex Dose Pack) may improve liver enzyme levels in some patients, but it is hepatotoxic and should be used cautiously. The general application of toxic immunosuppressive agents should await the results of large, long-term, prospective trials. Liver transplantation is the only proven effective therapy for advanced, decompensated PSC and PBC.
Consistent regression of intestinal metaplasia in Barrett's esophagus has not been achieved with medical or surgical interventions. In this case report, a patient with Barrett's esophagus of stable length had half the circumference of the Barrett's epithelium ablated with laser therapy while on a high-dose proton-pump inhibitor. In the absence of esophageal acid exposure and after laser ablation, the intestinal metaplasia was documented to reepithelialize with normal squamous mucosa, which has persisted.
Barrett's oesophagus is receiving increasing scrutiny as the rates of adenocarcinoma of the oesophagus rise. Because clinical features are not predictive of the presence of Barrett's oesophagus and most individuals with Barrett's oesophagus go undetected, a case can be made for surveillance endoscopy in patients with chronic reflux. Once Barrett's oesophagus is diagnosed patients should be entered into a surveillance programme despite lack of proof of efficacy. Scientific study of putative biological markers of increased risk has added dramatically to the understanding of the biology of the lesion, but currently the finding of high grade dysplasia remains the best marker predicting the presence of greatly increased risk of developing cancer. It is likely that newer molecular biology techniques will become clinically applicable biological markers in the future. Currently there is no effective medical nor surgical therapy to cause regression of the metaplastic Barrett's epithelium, however the application of novel de-differentiating agents or ablation of the metaplastic epithelium while controlling oesophageal acid exposure and other environmental abnormalities offer hope that effective treatment of Barrett's oesophagus may someday be reality.
UNLABELLED: In this study, our objective was to determine whether 6 months of open-label therapy with sulindac 400 mg/daily or piroxicam 20 mg/daily promote regression of adenomatous colonic polyps left in situ. Left-sided colonic polyps (size 3-12 mm) detected at colonoscopy were measured and left without being biopsied. The bowel wall opposite to the polyps was marked with India ink submucosally. Patients were assigned to drug therapy, and compliance was determined by pill count. Polyps were measured during sigmoidoscopy after 3 and 6 months of treatment; polyps were removed at the 6-month examination. Examiners were not blinded to drug therapy or previous polyp measurements. Seven patients completed 6 months of therapy (five sulindac and two piroxicam). Two additional patients treated with piroxicam were withdrawn secondary to adverse events (bleeding gastric ulcer and rash). In one patient treated with sulindac, a 6-mm polyp disappeared, and two other polyps seemed to regress partially. One polyp regressed partially in a piroxicam-treated patient. All other polyps remained unchanged. CONCLUSIONS: We did not observe dramatic regression of sporadic colon adenomatous polyps to either sulindac or piroxicam after 6 months of therapy in this small uncontrolled pilot study.
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