Collagenous colitis: oral low-dose methotrexate for patients with difficult symptoms: long-term outcomes.

AIM: To perform a qualitative retrospective review of identified cases of collagenous colitis within the patient databases of local clinicians, with particular attention to the use and effectiveness of oral low-dose methotrexate. METHODS: Gastroenterologists in the referral area were invited to identify collagenous colitis cases from their own databases for inclusion in the study. Patients were considered eligible if they had a symptom history and colonic mucosal histology consistent with collagenous colitis. The retrospective analysis identified age at diagnosis, previous therapies, date of commencement and duration and effectiveness of methotrexate, side-effects, and repeat colonic mucosal histology (if available) after a period of treatment. RESULTS: Between 1986 and 2003, 43 eligible patients were identified, ranging in age from 32 years to 88 years at the time of diagnosis. Nineteen of the 43 received methotrexate over varying periods, and in 16 of these the clinical response was considered either 'Good' (14) or 'Partial' (2). In the methotrexate group 10 of the 19 underwent repeat colonoscopy and mucosal biopsy at some stage after commencing methotrexate. Of these, five had normal histology in comparison with pretreatment abnormal histology, two had improvement but not normalization of histology, and three had unchanged abnormal histology. CONCLUSION: The data from this retrospective review suggest that methotrexate may have a beneficial effect on symptoms of collagenous colitis and may improve the underlying histological abnormality. A controlled trial of adequate power and duration is needed to further clarify the usefulness of methotrexate in this condition.

Proton-pump inhibitor therapy and the development of dysplasia in patients with Barrett's oesophagus.

OBJECTIVE: To examine whether proton-pump inhibitor (PPI) therapy influences the incidence and progression of dysplasia in patients with Barrett's oesophagus. DESIGN AND SETTING: Review of prospective data on patients undergoing surveillance with regular endoscopy and biopsy at a private endoscopy centre in Canberra, ACT, between 1981 and 2001. PATIENTS: 350 patients diagnosed with Barrett's oesophagus. INTERVENTIONS: PPI therapy was progressively introduced into clinical practice from late 1989. Once begun, PPI therapy was ongoing, with no attempt to reduce the dose. MAIN OUTCOME MEASURES: Relationship between development of dysplasia or adenocarcinoma and delay between diagnosis with Barrett's oesophagus and starting PPI therapy was determined by Cox regression analyses, stratified by year of enrollment. Age, sex, presence of macroscopic markers (severe oesophagitis, nodularity, Barrett's ulcer, stricture) and use of aspirin or non-steroidal anti-inflammatory drugs were considered as confounding factors in the regression analyses. RESULTS: The 350 patients had 1422 surveillance endoscopies, with a median follow-up of 4.7 years. Patients who delayed using a PPI for 2 years or more after diagnosis with Barrett's oesophagus had 5.6 times (95% CI, 2.0-15.7) the risk of developing low-grade dysplasia at any given time as those who used a PPI in the first year. Similar results were found for the risk of developing high-grade dysplasia or adenocarcinoma (hazard ratio, 20.9; 95% CI, 2.8-158). CONCLUSIONS: Use of ongoing PPI therapy appeared beneficial in the prevention of dysplasia and adenocarcinoma in patients with Barrett's oesophagus. We suggest that all patients with this condition, even those with no oesophagitis or symptoms, should be encouraged to continue long term PPI therapy.

Barrett's esophagus: Macroscopic markers and the prediction of dysplasia and adenocarcinoma.

BACKGROUND AND AIMS: Surveillance endoscopy has been advocated for patients with Barrett's esophagus but the cost-effectiveness of this has been questioned. The aim of this study is to identify an optimum surveillance protocol by examining if macroscopic markers at diagnosis predict the development of dysplasia. METHODS: The sample was 353 patients with Barrett's esophagus undergoing surveillance by a community-based group of gastroenterologists between 1981 and 2001. At diagnosis the presence of macroscopic and microscopic markers was noted. The presence and pattern of dysplasia and development of adenocarcinoma was documented during subsequent surveillance. RESULTS: Three hundred and fifty-three patients (71% male) underwent regular surveillance over 19 056 patient-months (median 42 months), having a median number of three surveillance endoscopies (range 1-40). Nine patients (seven male) developed adenocarcinoma (1/176 patient years) and four male patients developed high-grade dysplasia (1/397 patient years). Twelve of these 13 patients entered with one or more macroscopic markers: severe esophagitis, nodularity, Barrett's ulcer or stricture. Dysplasia risk was associated with macroscopic markers. Patients who entered with one marker were 6.7 times more likely to develop high-grade dysplasia/adenocarcinoma (HR = 6.7, 95% CI = 1.3, 35). Patients who entered with two or more markers were 14 times more likely to develop high-grade dysplasia/adenocarcinoma (HR = 14.1, 95% CI = 2.02, 102). CONCLUSIONS: The presence of severe esophagitis, Barrett's ulcer, nodularity or stricture at entry indicates a high-risk group for Barrett's esophagus. Cost-effectiveness of surveillance for these patients and those with dysplasia at entry would thus improve.

Sedation for endoscopy: the safe use of propofol by general practitioner sedationists.

OBJECTIVE: To determine the incidence of adverse events related to an endoscopy sedation regimen that included propofol, delivered by general practitioner (GP) sedationists. DESIGN: Audit of reports of sedation-related adverse events in patients undergoing endoscopy. A sample of 1000 patients' medical records was also reviewed to determine the drugs and dosages used and the proportion of sedations delivered by GPs. SETTING AND PARTICIPANTS: All patients undergoing gastroscopy and/or colonoscopy from January 1996 to December 2000 in two private endoscopy centres in Canberra. Sedation was provided by GPs or a specialist anaesthetist, in most cases using a drug regimen that included propofol. MAIN OUTCOME MEASURES: Incidences of respiratory arrest, airway obstruction, hypoxia requiring intervention, hypotension, and death; number of interventions to correct these events, including extra airway management, bag-mask ventilation, intravenous fluid infusion, endotracheal intubation and the use of reversal agents, and admission to hospital. RESULTS: 28,472 procedures were performed in the five years. There were 185 sedation-related adverse events (6.5/1000 procedures; 95% CI, 5.6-7.4): 107 for airway or ventilation problems (3.8/1000) and 77 hypotensive episodes (2.7/1000). Respiratory-related adverse events were more common in patients managed by GPs than anaesthetists, but this was not significant (P = 0.1). Interventions were recorded in 234 patients (8.2/1000; 95% CI, 7.2-9.3): 123 to maintain ventilation, and 111 intravenous infusions. GPs were more likely than anaesthetists to intervene to manage respiratory-related adverse events (P = 0.03). Four patients required transfer or admission to hospital. No patients required endotracheal intubation, and there were no deaths. CONCLUSIONS: The GP sedationists encountered a low incidence of adverse events, which they managed effectively. It appears that appropriately selected and trained GPs can safely use propofol for sedation during endoscopy.