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Background & Aims: Outcomes of colon surveillance after colorectal cancer screening with colonoscopy are uncertain. We conducted a prospective study to measure incidence of advanced neoplasia in patients within 5.5 years of screening colonoscopy. Methods: Three thousand one hundred twenty-one asymptomatic subjects, age 50 to 75 years, had screening colonoscopy between 1994 and 1997 in the Department of Veterans Affairs. One thousand one hundred seventy-one subjects with neoplasia and 501 neoplasia-free controls were assigned to colonoscopic surveillance over 5 years. Cohorts were defined by baseline findings. Relative risks for advanced neoplasia within 5.5 years were calculated. Advanced neoplasia was defined as tubular adenoma greater than ≥10 mm, adenoma with villous histology, adenoma with high-grade dysplasia, or invasive cancer. Results: Eight hundred ninety-five (76.4%) patients with neoplasia and 298 subjects (59.5%) without neoplasia at baseline had colonoscopy within 5.5 years; 2.4% of patients with no neoplasia had interval advanced neoplasia. The relative risk in patients with baseline neoplasia was 1.92 (95% CI: 0.83–4.42) with 1 or 2 tubular adenomas <10 mm, 5.01 (95% CI: 2.10–11.96) with 3 or more tubular adenomas <10 mm, 6.40 (95% CI: 2.74–14.94) with tubular adenoma ≥10 mm, 6.05 (95% CI: 2.48–14.71) for villous adenoma, and 6.87 (95% CI: 2.61–18.07) for adenoma with high-grade dysplasia. Conclusions: There is a strong association between results of baseline screening colonoscopy and rate of serious incident lesions during 5.5 years of surveillance. Patients with 1 or 2 tubular adenomas less than 10 mm represent a low-risk group compared with other patients with colon neoplasia. [Copyright &y& Elsevier]

Gastric ulcer disease remains a cause of hemorrhage, perforation, outlet obstruction, and death. Recent advances in the understanding of peptic ulcer disease indicate that infection with Helicobacter pylori and ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs) are the cause of almost all gastric and duodenal ulcers, Our therapy, therefore, is in a state of transition: the old acid-suppressive temporary therapy that allows frequent ulcer recurrences and complications is being replaced by curative therapies. The old therapy, by reducing gastric acid secretion or enhancing gastric mucosal defenses, inhibited the cofactors needed for ulcer development. Acid suppression relieved symptoms and healed ulcers, while defense enhancers, such as prostaglandin analogs healed and prevented acute NSAID-induced gastric ulcers. These benefits were maintained, however, only as long as acid-reducing agents or mucosal defense enhancers were continued. On the other hand, curative therapies (such as eradicating H. pylori infection and/or stopping the use of NSAIDs) eliminate the causes of ulcer. Curative combination regimens consisting of antibiotics, ranitidine bismuth citrate, bismuth, and proton pump inhibitors have been approved by the Food and Drug Administration. These new regimens can cure benign gastric ulcer. Unfortunately, we cannot always determine which gastric ulcers are benign, and concern about gastric cancer remains. All gastric ulcers therefore still require biopsy and histological examination. With new treatment regimens, the time may be rapidly approaching when ulcer disease will be "history." [ABSTRACT FROM AUTHOR]

Purpose: We conducted a randomized, double-blind, multicenter clinical trial to determine whether lansoprazole was superior to continued therapy with histamine H2-receptor antagonist therapy in healing erosive reflux esophagitis. Methods: Investigators from nine medical centers enrolled 159 patients with endoscopically documented esophageal erosions and/or ulcers that had failed to heal with 12 or more wk of at least standard dosages of histamine H2-receptor antagonist therapy. Patients received ranitidine 150 mg b.i.d. for 8 wk or lansoprazole 30 mg for 4 wk followed by either lansoprazole 30 mg or laasoprazole 60 mg for another 4 wk of treatment. Patients underwent endoscopy at screening and at weeks 2, 4, and 8. Results: At 2, 4, and 8 wk of therapy, healing rates were significantly higher in the lansoprazole group compared with the ranitidine group (p < 0.001). By 8 wk, 84% of the lansoprazole group were healed as opposed to only 32% of the ranitidine group. Lansoprazole was superior to ranitidine in providing relief of upper abdominal burning and daytime heartburn (p < 0.001) and reducing the need for antacids (p < 0.001). Lansoprazole patients had less interference with sleep and less daytime drowsiness than ranitidine patients (p = 0.05). The percentages of patients with adverse events were similar in both groups. Fasting serum gastrin levels at weeks 4 and 8 were significantly higher in the lansoprazole group compared with the ranitidine group. Conclusion: Eight weeks of lansoprazole therapy is safe, superior to continued ranitidine therapy, and effective in healing more than 80% of patients with erosive reflux esophagitis previously resistant to histamine H2-receptor antagonist therapy. [ABSTRACT FROM AUTHOR]

Objective: This randomized, double-blind study was designed to determine whether the proton pump inhibitor lansoprazole could prevent relapse among patients with healed erosive reflux esophagitis that had been resistant to healing with at least 3 months of H2-receptor antagonist therapy. Results: By the end of the year, 13% of placebo patients remained healed compared with 67% of lansoprazole 15 mg and 55% of lansoprazole 30 mg patients (p < 0.001 for time to first relapse). All placebo patients were symptomatic by the end of the study whereas only one-third of the lansoprazole patients was symptomatic at the end of the 12-month study period. The two lansoprazole doses were comparably effective in maintaining healing and in symptom control and were well tolerated. Fasting serum gastrin values increased significantly to about 1.5-2 times the baseline values over the first 2 months of lansoprazole treatment; no further increase was noted. Conclusion: Erosive relapse can be prevented in most patients for up to 1 yr with lansoprazole 15 mg or 30 mg once daily. [ABSTRACT FROM AUTHOR]

Objectives: This study was designed to compare lansoprazole 30 mg, lansoprazole 15 mg, omeprazole 20 mg, and placebo in the treatment of erosive reflux esophagitis. Methods: In a double-blind, multicenter study, 1284 patients with endoscopically diagnosed erosive reflux esophagitis were randomized to received lansoprazole 30 mg (n = 422), lansoprazole 15 mg (n = 218), omeprazole 20 mg (n = 431), or placebo (n = 213) once daily for 8 wk. At 2, 4, 6, and 8 wk, healing was evaluated endoscopically. Patients kept daily diaries of symptoms. Results: Healing rates at 2, 4, 6, and 8 wk were 65.3%, 83.3%, 89.4%, and 90.0%, respectively, for lansoprazole 30 mg: 56.3%, 74.6%, 80.3%, and 78.8% for lansoprazole 15 mg: 60.9%, 82.0%, 89.7%, and 90.7% for omeprazole 20 mg; and 23.9%, 32.8%, 36.6%, and 40.0% for placebo (all active treatments higher than placebo, p < 0.001). Healing rates with lansoprazole 30 mg were significantly higher than with lansoprazole 15 mg at all time points (p < 0.05). Healing rates with omeprazole 20 mg were significantly higher than with lansoprazole 15 mg at 4, 6, and 8 wk and were similar to those with lansoprazole 30 mg. Based on patient diaries, lansoprazole 30 mg produced better symptomatic relief than lansoprazole 15 mg or omeprazole 20 mg, primarily early in the treatment course. Conclusions: Both lansoprazole 30 mg and omeprazole 20 mg were more effective than lansoprazole 15 mg in esophageal mucosal healing. Compared with omeprazole 20 mg, lansoprazole 30 mg was as safe, was similarly effective with respect to esophageal healing, and provided superior symptomatic relief, primarily early in treatment. Lansoprazole 30 mg provided greater symptomatic relief than lansoprazole 15 mg. [ABSTRACT FROM AUTHOR]

Objective: Conventional ulcer therapy has not been proven effective in healing gastric ulcers caused by nonsteroidal anti-inflammatory drugs (NSAIDs) if the NSAIDs are continued. Our objective in this study was to determine whether a prostaglandin analog is an effective treatment for such NSAID-induced lesions. Methods: To make this determination, we conducted a 9-wk double-blind trial comparing placebo with enprostil 35 µg twice daily and three times daily. Use of antacids was not allowed. Three centers entered 145 patients with chronic inflammatory arthritis and osteoarthritis, mean age 63 yr, who required continuous fixed-dose NSAID therapy within the range of therapeutic dosage. The minimum entrance criterion was the presence of either four gastric erosions or one gastric ulcer. Two pretreatment endoscopies within a 2-wk interval were performed to establish the presence of stable baseline gastric lesions. Endoscopy was repeated at wk 6 and 9 during treatment. All groups were similar with regard to age distribution, sex, weight, height, smoking usage, and alcohol consumption. Results: The ulcer healing rates were 14%, 57%, and 68% at 6 wk and 19%, 68%, and 74% at 9 wk for the groups receiving placebo, enprostil twice daily, and enprostil three times daily, respectively (p < 0.01). Complete mucosal healing of all erosions and ulcers at 9 wk occurred in 59% of enprostil-treated patients and in 10% of placebo-treated patients. Additional gastric erosions and gastric ulcers developed in 16% of placebo patients and 4% of the enprostil patients. Eighteen percent of enprostil patients withdrew early from the study due to adverse experiences, such as diarrhea and abdominal pain. Conclusion: We concluded that during continued NSAID therapy 1) enprostil 35 µg (taken either twice daily or three times daily) heals NSAID-induced gastric ulcers and erosions and protects the mucosa from further NSAID-induced gastric injury; 2) gastric ulcers and erosions... [ABSTRACT FROM AUTHOR]

Focuses on clinical trials on maintenance therapy for peptic ulcer disease. Factors included in the long-term plan for ulcer disease management; Pharmacological intervention in duodenal ulcer recurrences; Effect of initial treatment on ulcer recurrence; Methods of analyzing maintenance trials.

Naturally occurring PGs are considered important in maintaining the integrity of the gastrointestinal mucosa. Evidence indicates that synthetic analogs of PGs heal gastroduodenal ulcers in doses that suppress gastric acid. No consistent benefit of this class of drugs compared with already available conventional agents has been demonstrated in the treatment of duodenal or gastric ulcer disease. Nonantisecretory doses of PGs, by maintaining mucosal integrity and preventing ulcer recurrence, may eventually have a role in the treatment of ulcer disease. The potential of PGs to prevent gastroduodenal mucosal injury caused by nonsteroidal anti-inflammatory, drugs, alcohol, aspirin, and stress, if supported by the results of ongoing clinical trials, may be a major therapeutic advance for the treatment of peptic ulcer and related acid peptic diseases. [ABSTRACT FROM AUTHOR]

Comments on various issues relevant to internal medicine. Medical effect of nuclear weapons; Therapeutic effect of granulocyte transfusions; Correlation between Raynaud's phenomenon and vinblastine-bleomycin therapy.

Discusses several issues concerning internal medicine. Information on late-onset 21-hydroxylase deficiency; Details on a case study of pancreatic carcinoma in brothers; Discussion on the incidence of campylobacter enteritis in Iceland.