Opportunistic screening of hospital staff using primary colonoscopy: participation, discomfort and willingness to repeat the procedure.

BACKGROUND: Participation in and tolerability of primary colonoscopy screening are presumed to be relatively low. The present study aimed to test its feasibility in a well-informed population of hospital staff using an intensive information campaign, and to identify factors associated with screening colonoscopy rated as uncomfortable. METHODS: Data were collected using standardized forms. RESULTS: Out of 1,090 invited employees (50-65 years), 447 (41.0%) participated. Bowel preparation and colonoscopy were rated as 'somewhat to very uncomfortable' by 79.5 and 21.9%, respectively. 96.3% of participants were willing to repeat colonoscopy in the future. Participants rating colonoscopy as uncomfortable were more likely unwilling to repeat the procedure (OR 8.026, CI 2.667-24.154). Multivariate analysis (age- and gender-adjusted) showed an association of colonoscopy rated as uncomfortable with: abdominal pain during colonoscopy (OR 3.185, CI 1.642-6.178), other pain (OR 2.428, CI 1.335-4.416), flatulence (OR 2.175, CI 1.219-3.881), embarrassment (OR 2.843, CI 1.350-5.989), abdominal pain after colonoscopy (OR 1.976, CI 1.041-3.751), and a prolonged procedure time (OR 1.000, CI 1.000-1.001). CONCLUSIONS: Acceptance of primary colonoscopy screening for colorectal neoplasia was high, although participants with symptoms during and after colonoscopy were more likely to rate colonoscopy as uncomfortable. This type of opportunistic screening procedure is suitable for the introduction of screening programs and may be useful in areas that have no access to population-based screening.

Influence of phenotype at diagnosis and of other potential prognostic factors on the course of inflammatory bowel disease.

OBJECTIVES: Disease course in inflammatory bowel disease (IBD) is variable and difficult to predict. To optimize prognosis, it is of interest to identify phenotypic characteristics at disease onset and other prognostic factors that predict disease course. The aim of this study was to evaluate such factors in a population-based IBD group. METHODS: IBD patients diagnosed between 1 January 1991 and 1 January 2003 were included. A follow-up questionnaire was developed and medical records were reviewed. Patients were classified according to phenotype at diagnosis and risk factors were registered. Disease severity, cumulative medication use, and "surgical" and "nonsurgical" recurrence rates were calculated as outcome parameters. RESULTS: In total, 476 Crohn's disease (CD), 630 ulcerative colitis (UC), and 81 indeterminate colitis (IC) patients were diagnosed. In CD (mean follow-up 7.6 years), 50% had undergone resective surgery. In UC (mean follow-up 7 years), colectomy rate was 8.3%. First year cumulative recurrence rates per 100 patient-years for CD, UC, and IC were 53, 44, and 42%, respectively. In CD, small bowel localization and stricturing disease were negative prognostic factors for surgery, as was young age. Overall recurrence rate was increased by young age and current smoking. In UC, extensive colitis increased surgical risk. In UC, older age at diagnosis initially increased recurrence risk but was subsequently protective. CONCLUSIONS: This population-based IBD study showed high recurrence rates in the first year. In CD, small bowel localization, stricturing disease, and young age were predictive for disease recurrence. In UC, extensive colitis and older age at diagnosis were negative prognostic predictors.

Development and Validation of a Patient-reported Score to Screen for Mucosal Inflammation in Inflammatory Bowel Disease.

BACKGROUND AND AIMS: Patient-reported outcome measures [PROMs] assessing inflammatory bowel disease [IBD] activity are of interest for monitoring in clinical practice, telemedicine systems, or trials. Different PROMs for follow-up of disease activity are available; however, none was developed with endoscopy as gold standard. The objective of this study was to develop and validate a PROM to predict endoscopic disease activity, following the recommendations of the Food and Drug Administration. METHODS: During development, 178 IBD patients undergoing a colonoscopy were asked to fill out 13 clinical questions derived from the literature. During endoscopy, inflammation was assessed with the simplified endoscopic score for Crohn's disease [CD] and the Mayo endoscopic subscore for ulcerative colitis [UC]. Based on correlation with endoscopic inflammation, questions were reduced to a total of six for CD and five for UC. The newly developed Monitor IBD At Home questionnaire [MIAH] was validated in an independent cohort of 135 CD and 131 UC patients. Additionally, diagnostic accuracy of the MIAH combined with a calprotectin home test [CHT] was assessed. RESULTS: The MIAH-CD includes questions on rectal bleeding, mucus, stool frequency, urgency, fatigue, and patient-reported disease activity. The MIAH-UC contains items on rectal bleeding, stool frequency, urgency, abdominal pain, and patient-reported disease activity. Both questionnaires showed to be valid, reliable, and responsive to changes. The MIAH and CHT combined had a sensitivity, specificity, negative predictive value [NPV], and positive predicitive value [PPV] of 96.7%, 66.7%, 94.7%, and 76.3% for CD and of 88.2%, 81.4%, 95.6%, and 60.0% for UC, respectively, compared with endoscopy. CONCLUSIONS: The MIAH is the first PROM developed to predict endoscopic inflammation in IBD patients. A combination of this questionnaire and a CHT shows excellent diagnostic accuracy to screen for patients who need further assessment of disease activity, and can be used in daily practice, telemedicine systems, and trials.

[Current surveillance policy for Barrett's oesophagus in the Netherlands]. / Huidig beleid bij de surveillance van de barrettslokdarm in Nederland.

OBJECTIVE: To gain more insight into current surveillance and treatment of patients with Barrett's oesophagus with the aim of developing new guidelines. DESIGN: Questionnaire. METHOD: In 2004, a questionnaire was sent to 337 physician-endoscopists who were all registered with the Netherlands Society of Gastroenterology. The questionnaire inventoried various aspects of surveillance and treatment of patients with Barrett's oesophagus. RESULTS: Of the 289 respondents (86%), 96% carried out surveillance or had it carried out, on at least a proportion of their patients with Barrett's oesophagus. A total of 258 respondents (89%) carried out the surveillance themselves. An endoscopic indication of the presence of Barrett's oesophagus was, for 31% of the respondents, enough reason to carry out surveillance of this condition irrespective of the results of pathological investigations. 75% applied an age limit for surveillance for Barrett's. The median age limit is 75 years (interquartile distance: 70-75) and 46% of the treating professionals limited themselves to patients who, on the basis of age and co-morbidity, may undergo oesophageal resection. The choice of treatment in early neoplasia, surgical or endoscopic, depends not only on the histological diagnosis, but also on the age and the co-morbidities of the patient. CONCLUSION: Surveillance of Barrett's oesophagus is widespread in the Netherlands, and in general is carried out in accordance with international guidelines. The possibilities of treating patients with high-grade dysplasia or intramucosal carcinoma of the oesophagus endoscopically, and of consulting external advisory bodies are still insufficiently utilized.

Combination therapy of sucralfate and cimetidine, compared with sucralfate monotherapy, in patients with peptic reflux esophagitis.

A double-blind multicenter, randomized study was performed in 70 patients with endoscopically documented reflex esophagitis. Patients were randomly given 1 g sucralfate four times a day or the combination of sucralfate 1 g three times a day and 400 mg cimetidine at night. After healing of the esophagitis, patients were randomly given either sucralfate maintenance 2 g daily or placebo for a period of six months. Endoscopy was performed at the beginning of the study, after eight weeks, and, in cases with no healing, after 16 weeks of therapy. Sixty-three of the 70 patients who initially entered the study could be evaluated after eight weeks. Both groups showed good symptomatic improvement, and no side effects necessitated withdrawal of subjects. Endoscopy showed complete healing in 19.4 percent of the sucralfate group and in 21.9 percent of the combination sucralfate and cimetidine group. Endoscopic improvement was found in 50 percent of the sucralfate group and in 50 percent of the combination group. After 16 weeks, 56 patients could be evaluated. In the sucralfate group, improvement was seen in 78.6 percent, and healing in 31 percent. For the combination group these values were 59.3 percent and 37 percent (not significant). Twenty-six patients entered the maintenance phase of the study; 15 received sucralfate and 11 received placebo. Evaluation of 20 patients after six months showed endoscopic and/or symptomatic relapse of esophagitis in three of 12 patients receiving sucralfate and in two of the eight patients receiving placebo. It is concluded that sucralfate monotherapy in patients with reflux-esophagitis is effective and comparable with a combination of sucralfate during the day and cimetidine at night. No difference was found between sucralfate and placebo in terms of the relapse rate of esophagitis during long-term treatment.

Twenty-four-hour intragastric acidity: 300 mg ranitidine b.d., 20 mg omeprazole o.m., 40 mg omeprazole o.m. vs. placebo.

BACKGROUND: There is considerable controversy about the degree of acid suppression that is optimal for the treatment of peptic disorders. AIM: To compare the effects of three different regimens that are reported to strongly inhibit acid secretion. METHODS: Intragastric 24-hour pH monitoring was performed in 11 healthy subjects in a randomized, multiple, cross-over, double-blind study. Each subject received four dose regimens, each for 2 weeks, in a random order. The regimens were: 300 mg ranitidine b.d., 20 mg omeprazole o.m., 40 mg omeprazole o.m., and placebo. RESULTS: The decrease in gastric acidity during the daytime and during the total 24-hour period by all three treatments was significantly greater than after placebo; a significant difference in acid inhibition was found between ranitidine and 40 mg omeprazole, but not between ranitidine and 20 mg omeprazole, nor between the two doses of omeprazole. During the night-time the decrease in gastric acidity by all three treatments was significantly greater than after placebo; no difference was seen between the two doses of omeprazole and ranitidine. For the time of pH greater than 3 we found no statistical difference between the various acid decreasing regimens. The pH remained significantly longer above 4 after ranitidine and the two doses of omeprazole compared with placebo, and also longer above 4 after 40 mg omeprazole compared with ranitidine, but not after 20 mg omeprazole compared with ranitidine, nor after the two different doses of omeprazole. CONCLUSIONS: Dosing with 300 mg ranitidine b.d., 20 mg omeprazole or 40 mg omeprazole is superior in gastric acid inhibition compared with placebo, when measured using 24-hour pH monitoring.

Treatment of reflux oesophagitis of moderate and severe grade with ranitidine or pantoprazole--comparison of 24-hour intragastric and oesophageal pH.

BACKGROUND: Proton pump inhibiting drugs strongly decrease gastric acid secretion and have proven more effective in the treatment of reflux oesophagitis than H2-receptor antagonists. METHODS: In a double-blind randomized trial, 24 patients with oesophagitis grade II (n = 15) and III (n = 9) were treated for 4 weeks with either ranitidine 150 mg b.d. (n = 13) or pantoprazole 40 mg o.m. (n = 11). Before the trial and on the last day of medication, 24-h intragastric pH and oesophageal pH profiles were performed. Healing was assessed by endoscopy. RESULTS: Pantoprazole increased median gastric pH from 1.7 to 3.9. Virtually no change in gastric pH was seen in the ranitidine group. Pantoprazole reduced the fraction time of pH < 4 in the oesophagus from 21% to 3% (P = 0.0005), and the median number of refluxes from 206 to 56 (P = 0.022). Oesophageal acid exposure was not decreased by ranitidine. Healing of the oesophagitis was seen in 6/11 cases after pantoprazole and in 3/13 cases after ranitidine (N.S.) CONCLUSION: In patients with oesophagitis of moderate and severe grade, pantoprazole 40 mg o.m. decreases intragastric acidity and gastro-oesophageal acid reflux more effectively than ranitidine 150 mg b.d.

Omeprazole in peptic ulcers resistant to histamine H2-receptor antagonists.

Eighteen patients with duodenal, gastric or jejunal ulcers, resistant to at least 3 months treatment with histamine H2-receptor antagonists, singly or in combination with other anti-ulcer drugs, were treated with 40 mg omeprazole once daily for up to 8 weeks. All ulcers healed, the majority within two weeks. After ulcer healing patients were given maintenance therapy with high doses of cimetidine or ranitidine. Of 15 patients on maintenance therapy with H2-receptor antagonists, 12 (80%) developed a relapse after a period ranging from 3 to 52 weeks. Two patients were lost to follow-up. After re-healing on 40 mg omeprazole, two patients were given 20 mg omeprazole daily as maintenance therapy but relapses occurred again after 14 and 26 weeks respectively. After re-healing on 40 mg omeprazole, these two patients and one additional patient received maintenance therapy with 40 mg omeprazole daily. At present these three patients have been relapse-free for periods varying from 16 to 52 weeks. No side effects were registered during treatment with omeprazole. It is therefore concluded that omeprazole is highly effective in healing refractory peptic ulcers and that omeprazole maintenance therapy may be useful for prevention of relapse. Patients are sometimes seen with peptic ulceration which appears resistant to therapy with histamine H2-receptor antagonists, colloidal bismuth subcitrate, sucralfate or pirenzepine, either given as monotherapy for a prolonged period of time or as combination therapy. Usually the reason for such therapeutic failure remains obscure. Whether virtually total abolition of acid secretion will allow ulcer healing in these circumstances is unknown.(ABSTRACT TRUNCATED AT 250 WORDS)

Non-Helicobacter pylori bacterial flora during acid-suppressive therapy: differential findings in gastric juice and gastric mucosa.

BACKGROUND: Intragastric growth of non-Helicobacter pylori bacteria commonly occurs during acid-suppressive therapy. The long-term clinical consequences are still unclear. AIM: To investigate the luminal and mucosal bacterial growth during gastric acid inhibition, in relation to the type and duration of acid-inhibitory treatment, as well as to concomitant H. pylori infection. METHODS: A total of 145 patients on continuous acid inhibition with either proton pump inhibitors (n=109) or histamine2-receptor antagonists (H(2)RAs, n=36) for gastro-oesophageal reflux disease, and 75 dyspeptic patients without acid inhibition (control group) were included. At endoscopy, fasting gastric juice was obtained for pH measurement and bacteriological culture. Gastric biopsy specimens were examined for detection of H. pylori (immunohistochemistry) and of non-H. pylori bacteria (modified Giemsa stain-positive and immunohistochemistry-negative at the same location). RESULTS: Non-H. pylori flora was detected in the gastric juice of 92 (41.8%) patients and in the gastric mucosa of 109 (49.6%) patients. In gastric juice, prevalence rate for non-H. pylori bacteria was higher in patients taking proton pump inhibitors than controls and those taking H(2)RAs (58.7% vs. 22.6% and vs. 30.6%, P < 0.0001 and P < 0.003, respectively), but did not differ statistically between H(2)RAs and controls. In gastric mucosa, prevalence rates for non-H. pylori bacteria were higher in patients taking proton pump inhibitors and H(2)RAs than in the controls (antrum: 46.9% and 48.6% vs. 25%, P < 0.05 for both; corpus: 52.2% and 56.8% vs. 23.7%, P < 0.001 for both), but did not differ between proton pump inhibitors and H(2)RAs. Both luminal and mucosal growth of non-H. pylori bacteria were significantly greater in H. pylori-positive than -negative patients taking proton pump inhibitors (P < 0.05 for both). Luminal growth of non-H. pylori flora increased with the intragastric pH level, whilst mucosal bacterial growth increased with the duration of acid inhibition. CONCLUSIONS: Non-H. pylori flora not only contaminates the gastric juice but also colonizes the gastric mucosa of a large proportion of patients treated long-term with acid inhibition. The relationship between H. pylori and non-H. pylori bacteria in the pathogenesis of atrophic gastritis and gastric cancer needs further elucidation.

Double gastric infection with Helicobacter pylori and non-Helicobacter pylori bacteria during acid-suppressive therapy: increase of pro-inflammatory cytokines and development of atrophic gastritis.

BACKGROUND: Long-term acid suppression may accelerate the development of atrophic gastritis in Helicobacter pylori-positive subjects. The pathogenetic mechanism remains unclear. AIM: To test the hypothesis that gastric double infection with H. pylori and non-H. pylori bacterial species-during acid suppression-may result in an enhanced inflammatory response, contributing to the development of atrophic gastritis. PATIENTS AND METHODS: A consecutive series of patients with gastro-oesophageal reflux disease undergoing treatment with proton pump inhibitors (n=113) or histamine2-receptor antagonists (H2-RAs) (n=37), and 76 non-treated dyspeptic controls were investigated. Gastric mucosal H. pylori and non-H. pylori bacteria, histological gastritis, H. pylori serology, and circulating interleukin (IL)-1beta, IL-6, and IL-8 were examined. RESULTS: Patients on acid suppression with either proton pump inhibitors or H2-RAs had a similar prevalence of H. pylori infection to the controls, but a higher prevalence of non-H. pylori bacteria (61% and 60% vs. 29%, P < 0.0001 and P < 0.002). Both the presence of H. pylori and non-H. pylori bacteria were independent risk factors of atrophic gastritis (antrum: relative risks (RRs), 10.1 and 5.07; corpus: RRs, 11.74 and 6.38). A simultaneous presence of H. pylori and non-H. pylori bacteria was associated with a markedly increased risk of atrophic gastritis (antrum: RR, 20.25; corpus: RR, 20.38), compatible with a synergistic effect. Furthermore, the simultaneous presence of both types of bacteria was associated with higher cytokine levels than in patients without any type of bacteria. This increase was also greater than in patients with H. pylori infection alone (P < 0.001, for both IL-1beta and IL-8). SUMMARY AND CONCLUSIONS: H. pylori-positive patients on long-term acid inhibition displayed three features: non-H. pylori bacterial growth; increased cytokine levels; and a higher risk of atrophic gastritis. We suggest that double infection with H. pylori and non-H. pylori bacteria is a major factor in the development of atrophic gastritis during gastric acid inhibition.

Serum gastrin and chromogranin A during medium- and long-term acid suppressive therapy: a case-control study.

BACKGROUND: Serum chromogranin A (CgA) is regarded as a reliable marker of neuroendocrine proliferation. We previously described increased serum CgA levels during short-term profound gastric acid inhibition. AIM: To investigate serum gastrin and CgA levels in dyspeptic patients during continuous medium- (6 weeks to 1 year), or long-term (1-8 years) gastric acid suppressive therapy. PATIENTS AND METHODS: 114 consecutive dyspeptic patients referred for upper gastrointestinal endoscopy were enrolled in a cross-sectional, case-control study [62 patients on continuous antisecretory therapy, either with proton pump inhibitors (n = 47) or H2-receptor antagonists (H2RA) (n = 15) for gastro-oesophageal reflux disease with or without Barrett's oesophagus or functional dyspepsia, and 52 age- and sex-matched patients without medical acid inhibition and with normal endoscopic findings (control group)]. Omeprazole doses ranged from 20 mg to 80 mg daily and ranitidine from 150 mg to 450 mg daily. Fasting serum CgA and serum gastrin levels were measured by radioimmunoassay (reference values: serum CgA < 4.0 nmol/L; serum gastrin < 85 ng/L). RESULTS: Fasting serum CgA levels positively correlated with serum gastrin in the entire study population (r = 0. 55, P = 0.0001). Median serum CgA values were higher in patients treated with a proton pump inhibitor than H2RA [2.8 (2.0-5.9) nmol/L vs. 2 (1.9-2.3) nmol/L, P < 0.002] and controls [2.8 (2.0-5.9) nmol/L vs. 1.8 (1.5-2.2) nmol/L, P < 0.0001) and did not differ between patients treated with H2RA or controls. Serum gastrin and CgA levels in patients on proton pump inhibitor therapy positively correlated with the degree and duration of acid inhibition. Patients on long-term proton pump inhibitor therapy had significantly higher fasting serum gastrin and CgA than those on medium-term proton pump inhibitor therapy [127 (73-217) ng/L vs. 49 (29-78) ng/L, P < 0.0001 and 4.8 (2.8-8) ng/L vs. 2.1 (1.9-2.6) ng/L, P < 0.001]. No such relation was found in patients on medium- vs. long-term H2RA. Overall, patients with positive Helicobacter pylori serology had higher serum gastrin and CgA levels than those with negative H. pylori serology [51 (27-119) ng/L vs. 27 (14-79) ng/L, P = 0.01, 2.4 (1.9-3.4) nmol/L vs. 2.0 (1.7-2.5) nmol/L, P = 0.05]. CONCLUSIONS: During long-term continuous proton pump inhibitor treatment, serum gastrin and CgA levels are significantly elevated compared to H2RA treatment and nontreated dyspeptic controls. H. pylori infection seems to affect gastric ECL cell secretory function. Increased serum CgA values during long-term profound gastric acid inhibition could reflect either gastric enterochromaffin-like cell hyperfunction or proliferative changes.

Barrett's oesophagus.

Barrett's oesophagus or columnar lined epithelium of the oesophagus (CLO) is a metaplastic condition associated with excessive gastro-oesophageal reflux. It is found in 15% of patients with reflux oesophagitis. In a detailed study of 115 CLO patients dysplasia was found in 46%; 13.9% were moderate or severe dysplasia, usually found in intestinal type CLO. Fifty patients were endoscoped annually to determine the natural history of the disease. The incidence of adenocarcinoma was 1 in 52 patient-years, a 125-fold excess risk. A dysplasia-carcinoma sequence was seen in the five who developed carcinoma. Patients with early carcinoma were treated surgically with 12% postoperative mortality and 100% survival for 24-70 months.

Changes in gastric mucosa and luminal environment during acid-suppressive therapy: a review in depth.

Acid-suppressive therapy and subsequent changes in gastric mucosa and luminal environment rank highly amongst the investigated issues in gastroenterology over the past two to three decades. Herewith, we present an overview of these intragastric changes, particularly during long-term administration of acid-suppresive medication and concurrent infection with Helicobacter pylori. Current evidence indicates that: i) Long-term acid suppression facilitates the development of fundic ECL cell hyperplasia, especially in the presence of Helicobacter pylori. No neoplastic changes directly attributable to acid suppression have so far been demonstrated in humans. ii) Acid-suppressive therapy increases the risk of enteric infections. iii) Acid-suppressive therapy does not alter fat and mineral bioavailability, but may decrease the absorption of protein-bound vitamin B12. iv) Acid suppression invariably results in intragastric overgrowth of non-Helicobacter pylori bacterial species. The concurrent infection with Helicobacter pylori may promote this bacterial overgrowth and the intragastric formation of N-nitrosamines. v) Acid-suppressive therapy alters the natural course of Helicobacter pylori gastritis, transforming the antral-predominant pattern into a body-predominant pattern, which in turn may progress to body gland atrophy. The pathophysiology of this phenomenon is currently under investigation. vi) In view of the potential adverse effects of acid suppression in the presence of Helicobacter pylori, the screen-and-treat strategy is advocated for Helicobacter pylori in subjects considered for long-term treatment.

Cardiopulmonary events during primary colonoscopy screening in an average risk population.

BACKGROUND: Large colorectal cancer screening studies using primary colonoscopy have reported a low risk of major complications. Studies on diagnostic and therapeutic colonoscopy have pointed to a frequent occurrence of(minor) cardiopulmonary events, and with the steady increase of colonoscopy screening, it is important to investigate their occurrence in colonoscopy screening. METHODS: This study describes the frequency of bradycardia(pulse rate <60 min-1), hypotension (systolic blood pressure(SB P) <90 mmHg), hypoxaemia (blood oxygenation, SaO2<90%) and ECG changes during colonoscopy screening in an average-risk population (hospital personnel, n=214,mean age 54.0±3.8, 39.3% male), without significant comorbidity) and aims at identifying subject-related and/or endoscopic factors associated with their occurrence. All data were collected prospectively. During 214 consecutive primary screening colonoscopies under conscious sedation(midazolam and pethidine), on top of pulse rate and SaO2,blood pressure and a three-channel ECG were recorded every five minutes. RESULTS: No major complications or relevant ECG changes occurred. Hypoxaemia occurred in 119 (55.6%),hypotension in 19 (8.9%) and bradycardia in 12 subjects(5.6%). In multivariate analysis, the sedation level 3 increased the risk of hypoxaemia (OR 4.8, CI 1.7-13.7), and incomplete colonoscopy (OR 5.3, CI 1.6-18.1) was associated with hypotension. Subjects with bradycardia had a longer mean procedure time (38±12 vs. 29±12 min, p<0.05), which did not turn out as a risk factor in a multivariate analysis. CONCLUSIONS: Mainly procedure-related and not subject-related factors were found to be associated with the occurrence of cardiopulmonary events in primary colonoscopy screening in this relatively healthy screening population.

Fatigue and health-related quality of life in inflammatory bowel disease: results from a population-based study in the Netherlands: the IBD-South Limburg cohort.

BACKGROUND: The importance of fatigue in chronic disease has been increasingly recognized; however, little is known about fatigue in inflammatory bowel disease (IBD). The aim of the present study was to investigate the prevalence and severity of fatigue and the impact on health-related quality of life (HRQoL) in patients included in a population-based IBD cohort in the Netherlands. METHODS: IBD patients, diagnosed between January 1st, 1991, and January 1st, 2003, were followed up for a median of 7.1 years. They completed a questionnaire, which included a disease activity score, the Multidimensional Fatigue Inventory (MFI-20), the Inflammatory Bowel Disease Questionnaire (IBDQ), and the Short Form health survey (SF-36). Hemoglobin levels were recorded. RESULTS: Data were available in 304 Crohn's disease (CD), 368 ulcerative colitis (UC), and 35 indeterminate colitis (IC) patients. During quiescent disease, the prevalence of fatigue was nearly 40%. MFI-20 and HRQoL scores were significantly worse in IBD patients having active disease. In a multivariate analysis, disease activity was positively related with the level of fatigue in both CD and UC. In UC, anemia influenced the general fatigue score independently of disease activity. Disease activity as well as fatigue were independently associated with an impaired IBDQ. CONCLUSIONS: In IBD, even in remission, fatigue is an important feature. Both in CD and in UC, fatigue determined HRQoL independently of disease activity or anemia. This implies that in IBD patients physicians need to be aware of fatigue in order to better understand its impact and to improve the HRQoL.

Clinical studies of sucralfate in reflux esophagitis. The European experience.

Reflux esophagitis is encountered quite frequently in clinical practice. Symptoms can be mild, moderate, or severe and complications can occur, particularly if the disorder is untreated or undertreated. Treatment is aimed at relieving symptoms, healing lesions, and preventing complications. Various pharmacologic options are available for treatment, including antacids, alginate/antacid compounds, acid-reducing agents, prokinetic drugs, and agents that protect the mucosa. This article reviews a number of clinical studies evaluating sucralfate in the treatment of reflux esophagitis. Almost all of the investigations were conducted in Europe and encompassed open-label studies, placebo-controlled trials, and comparative studies. From the studies discussed, it can be concluded that sucralfate not only has a place in the treatment of peptic ulcer disease, but is also effective in treating reflux esophagitis. Sucralfate is comparable to H2-receptor antagonists in symptom improvement and healing rates. In addition, the studies reviewed have shown sucralfate to be safe and well tolerated.

Healing of chronic Barrett ulcers with omeprazole.

Three patients with a long-standing benign Barrett ulcer, resistant to treatment with high doses of either cimetidine or ranitidine, given for at least 3 months, were treated with 40 mg omeprazole daily for 9 wk. After 2 wk all symptoms had disappeared and at the end of treatment all three patients showed complete endoscopic ulcer healing. Patient compliance was excellent and no side effects were registered. We conclude that omeprazole is effective and safe in healing chronic resistant Barrett ulcers.