bluuebunny/crossref_metadata_2025_split huggingface dataset:
13C‐urea breath test without a test meal is highly accurate for the detection of Helicobacter pylori infection in Chinese
Authors: Wong W. M. , Wong B. C. Y. , Wong K. W. , Fung F. M. Y. , Lai K. C. , Hu W. H. C. , Yuen S. T. , Leung S. Y. , Lau G. K. K. , Lai C. L. , Chan C. K. , Go R. , Lam S. K. 
Published: March 2003

Background:Conventional 13C‐urea breath testing (13C‐UBT) includes a test meal to delay gastric emptying, which, theoretically, improves the accuracy of the test. Citric acid has been proposed as the best test meal. However, recent studies have suggested that a test meal may not be necessary.Aim:To investigate a new 13C‐UBT protocol without a test meal in a Chinese population.Methods:Consecutive dyspeptic patients referred for upper endoscopy were recruited. 13C‐UBT was performed on two separate days with or without a test meal (2.4 Gm citric acid) and compared with the ‘gold standard’ (CLO test and histology).Results:Two hundred and two patients were tested. Using receiver operating characteristics (ROC) analysis, the optimal delta‐value and optimal measurement interval for UBT were 5% and 30 min, respectively, both with or without a test meal. The sensitivity, specificity, positive predictive value, negative predictive value and accuracy of 13C‐UBT with citric acid (96.5%, 97.7%, 98.2%, 95.6%, 97.0%) were similar to 13C‐UBT without a test meal (94.7%, 97.7%, 98.2%, 93.5%, 96.0%).Conclusion:This simplified 13C‐UBT protocol without a test meal produced highly accurate and reliable results in the Chinese population.
Low serum retinol levels are associated with hepatocellular carcinoma in patients with chronic liver disease
Authors: Newsome P. N. , Beldon I. , Moussa Y. , Delahooke T. E. , Poulopoulos G. , Hayes P. C. , Plevris J. N. 
Published: March 2003

Background:Retinol and other vitamin A derivatives affect the differentiation and growth of many tissues and have anti‐tumour properties.Aim:To investigate serum retinol levels in patients with liver disease and hepatocellular carcinoma (HCC) and to assess its importance as a risk factor for the development of HCC.Methods:Serum retinol levels were measured in healthy volunteers and 175 patients (34 with chronic hepatitis C, 117 with cirrhosis, and 24 with HCC.Results:The serum retinol levels (mean ± s.e.) in ng/mL, were 972.1 ± 37.7 in the control group and 647 ± 41.1 in patients with chronic hepatitis C. Serum retinol levels in patients with cirrhosis and HCC were lower than in patients with cirrhosis alone (365.8 ± 43.1 vs. 438.9 ± 22.1, P < 0.04). In particular, there was a more significant difference in serum retinol levels between Child–Pugh grade A patients with cirrhosis and Child–Pugh grade A patients with cirrhosis/HCC (serum retinol levels 532.4 ± 26.7 vs. 366.1 ± 86.4, P < 0.03). There was a significant difference in serum retinol levels between normal controls and all patients’ groups (P < 0.001). There were significantly lower serum retinol levels in cholestatic Child–Pugh grade A patients with cirrhosis compared with noncholestatic Child–Pugh grade A patients with cirrhosis/HCC (411.5 ± 30.3 vs. 579.7 ± 32.7, P < 0.0004). Sixty percent of patients with Child–Pugh grade A cirrhosis/HCC had serum retinol levels below 350 ng/mL compared with only 18.4% of cirrhotics without HCC (χ2‐test, P=0.01). No correlation was found between serum retinol levels and αFP or any other liver function tests, apart from serum albumin, which showed a positive correlation (r=0.61 P < 0.018).Conclusions:There was a progressive reduction in serum retinol levels from controls to patients with liver cirrhosis. Those patients with cirrhosis and HCC had significantly lower values than patients with cirrhosis alone. Serum retinol levels may be a risk factor for the development of HCC.
The effect of inflammation severity and of treatment on the production and release of TNFα by colonic explants in inflammatory bowel disease
Authors: Dionne S. , Ruemmele F. M. , Laberge S. , Seidman E. G. 
Published: March 2003

Background:Despite its pivotal role in mucosal inflammation, data on TNFα levels in inflammatory bowel diseases have been contradictory.Aim:To examine TNFα production in relation to the type and severity of inflammation and therapy, using colonic explant cultures.Materials and methods:Rectal mucosal biopsies from 271 paediatric patients (178 inflammatory bowel disease, 27 inflammatory controls, 66 normal) were cultured for 4 or 18 h. Basal TNFα tissue content and release into the medium were measured by ELISA and compared to histological severity and clinical parameters.Results:TNFα release as well as tissue‐associated TNFα levels were significantly increased in rectal biopsies from involved inflammatory bowel disease tissue. The amount of TNFα correlated with inflammation severity scores. TNFα levels were higher at 18 compared to 4 h in all groups, whether inflamed or not. TNFα released from rectal biopsies was lower among treated patients at 18 h. The presence of proximal colonic involvement was associated with higher TNFα release by uninvolved Crohn’s disease rectal biopsies compared to patients with ileitis alone.Conclusions:TNFα production and release is increased in involved rectal explants from inflammatory bowel disease. Anti‐inflammatory treatment diminishes this response.
Review article: chronic inflammation and reactive oxygen and nitrogen metabolism – implications in DNA damage and mutagenesis
Authors: Grisham M. B. , Jourd'Heuil D. , Wink D. A. 
Published: March 2003

SummaryIt is well known that chronic inflammation of the digestive tract is associated with an increased risk of malignant transformation. Because phagocytic leukocytes and cytokine‐activated parachymal cells produce large amounts of reactive metabolites of oxygen and nitrogen, there has been substantial interest in ascertaining whether these reactive intermediates may mediate mutagenesis and malignant transformation in vivo. However, very little information is available regarding the basic chemistry of how these oxygen and nitrogen‐derived species may interact to yield potentially carcinogenic agents. This review will discuss our present understanding of the chemical and biochemical interactions between superoxide and nitric oxide and provide a model by which these reactive species may damage DNA and mediate mutagenesis.
A new mechanism for anti‐inflammatory actions of proton pump inhibitors – inhibitory effects on neutrophil–endothelial cell interactions
Authors: Yoshida N. , Yoshikawa T. , Tanaka Y. , Fujita N. , Kassai K. , Naito Y. , Kondo M. 
Published: March 2003

Summary Background: Neutrophil–endothelial cell interactions mediated by adhesion molecules may be involved in gastric mucosal inflammation associated with Helicobacter pylori or nonsteroidal anti‐inflammatory drugs. Aim: To investigate the effects of proton pump inhibitors and histamine‐2 receptor antagonists (HRA) on neutrophil‐endothelial cell adhesive interactions induced by H. pylori water extract (HPE) or interleukin‐1β (IL‐1β). Methods: Human peripheral neutrophils and umbilical vein endothelial cells were incubated with either proton pump inhibitors (lansoprazole and omeprazole) or HRA (famotidine and ranitidine). Neutrophil surface expression of CD11b and CD18 and endothelial cell intercellular adhesion molecule‐1 (ICAM‐1) and vascular adhesion molecule‐1 (VCAM‐1) were assessed by flow cytometry and an enzyme immunoassay, respectively. Neutrophil adherence was defined as the ratio of exogenous neutrophils that adhered to the endothelial monolayers. Results: The expression of CD11b and CD18 on neutrophils and neutrophil‐dependent adhesion to endothelial cells elicited by HPE were inhibited by lansoprazole and omeprazole at clinical relevant doses, and the expression of ICAM‐1 and VCAM‐1 on endothelial cells and endothelial‐dependent neutrophil adherence induced by IL‐1β were also inhibited by lansoprazole and omeprazole at similar doses. Famotidine and ranitidine had no effect on neutrophil–endothelial cell interactions. Conclusions: These results indicate that proton pump inhibitors can attenuate neutrophil adherence to endothelial cells via inhibiting the expression of adhesion molecules, suggesting that proton pump inhibitors may have anti‐inflammatory activity.
Oesophageal transit, disintegration and gastric emptying of a film‐coated risedronate placebo tablet in gastro‐oesophageal reflux disease and normal control subjects
Authors: Perkins A. C. , Wilson C. G. , Frier M. , Blackshaw P. E. , Juan D. , Dansereau R. J. , Hathaway S. , Li Z. , Long P. , Spiller R. C. 
Published: March 2003

Background:Risedronate sodium is a pyridinyl bisphosphonate, proven effective for the treatment and prevention of postmenopausal osteoporosis and glucocorticoid‐induced osteoporosis and Paget’s disease of the bone.Aim:To compare the oesophageal transit, disintegration and gastric emptying of the commercial film‐coated risedronate tablet in subjects with gastro‐oesophageal reflux disease (GERD) and normal control subjects.Methods:A total of 30 subjects, 15 patients with GERD and 15 age‐ and sex‐matched, normal control subjects, participated in a single‐centre, open‐label, comparative gamma scintigraphy study. The GERD subjects had active erosive oesophagitis within 4 weeks prior to dosing.Results:The mean oesophageal transit (GERD, 4.4 s; controls, 3.1 s), mean disintegration (GERD, 21.8 min; controls, 19.2 min) and mean gastric emptying (GERD, 15.9 min; controls, 15.0 min) were similar in the two subject groups. The oesophageal transit is rapid and given the rapid disintegration and gastric emptying, oesophageal contact occurring via reflux of risedronate was unlikely since most, if not all, of the dosage form exited from the stomach within 30 min.Conclusions:The oval shape and film‐coating on the commercial risedronate tablet promotes rapid oesophageal transit and minimizes oesophageal contact, even in the high‐risk GERD population.
Effect of caloric density of a meal on lower oesophageal sphincter motility and gastro‐oesophageal reflux in healthy subjects
Authors: Pehl C. , Pfeiffer A. , Waizenhoefer A. , Wendl B. , Schepp W. 
Published: March 2003

Background:Patients with gastro‐oesophageal reflux disease are advised to avoid the ingestion of large meals. In healthy volunteers, a relationship between the amount of postprandial gastro‐oesophageal reflux and the volume of a liquid meal has been demonstrated.Aim:To evaluate whether the amount of postprandial gastro‐oesophageal reflux is also related to the calorie content of a meal, a second parameter that will be reduced by avoidance of the ingestion of large meals.Methods:Twelve healthy volunteers (six female, 19–31 years) received two solid–liquid meals with either 842 kcal (solid 582 kcal, liquid 260 kcal) or 582 kcal (31% reduction) in a randomized order. The nutritional components (10% fat, 76% carbohydrates, 14% protein) and the volume of the meals were identical in both meals. The lower oesophageal sphincter pressure was measured continuously in the first postprandial hour with a Dent sleeve, and pH‐metry was performed for 3 h postprandially with a glass electrode in the distal oesophagus. Blinded to the type of ingested meal, we calculated the mean lower oesophageal sphincter pressure, the frequency of transient lower oesophageal sphincter relaxations, the number of reflux episodes, and the fraction of time for which pH < 4.Results:A similar decrease in lower oesophageal sphincter pressure was observed after ingestion of the high calorie meal (median 10.9 mmHg, range 4.8–16.7 mmHg) and low calorie meal (median 9.9 mmHg, range 3.9–18.4 mmHg). No difference in the number of transient lower oesophageal sphincter relaxations (high calorie: median 9 per hour, range 5–13 per hour; low calorie: median 7 per hour, range 0–14 per hour) and of reflux episodes (high calorie: median 12 in 3 h, range 3–22 in 3 h; low calorie: median 12 in 3 h, range 3–30 in 3 h) was registered after intake of both types of meal. Additionally, no difference was identified regarding the fraction of time for which pH < 4 between the high calorie (mean 2.3%, 0.2–23.7%) and low calorie meal (3.3%, 0.5–17.8%).Conclusion:Reducing the caloric density of a meal neither influences postprandial lower oesophageal sphincter pressure nor decreases gastro‐oesophageal reflux in healthy volunteers. Thus, the amount of gastro‐oesophageal reflux induced by ingestion of a meal seems to depend on the volume but not on the caloric density of a meal.
Barrett’s oesophagus, dysplasia and pharmacologic acid suppression
Authors: Fitzgerald R. C. , Lascar R. , Triadafilopoulos G. 
Published: March 2003

Barrett’s oesophagus, a significant complication of gastro‐oesophageal reflux disease (GERD), is the single most important risk factor for oesophageal adenocarcinoma. The strong association between Barrett’s oesophagus and chronic GERD suggests that abnormal oesophageal acid exposure plays an important role in this condition. The progression of Barrett’s oesophagus from specialized intestinal metaplasia to dysplasia and finally invasive carcinoma is incompletely understood, but increased and disordered proliferation is a key cellular event. In ex vivo organ culture experiments, cell proliferation is increased after exposure to short pulses of acid, whilst proliferation is reduced in Barrett’s oesophagus specimens taken from patients with oesophageal acid exposure normalized by antisecretory therapy.In long‐term clinical studies, consistent and profound intra‐oesophageal acid suppression with proton pump inhibitors decreases cell proliferation and increases differentiation in Barrett’s oesophagus, but the clinical importance of such favourable effects on these surrogate markers is not clear. In clinical practice, proton pump inhibitors relieve symptoms and induce partial regression to squamous epithelium, but abnormal oesophageal acid exposure and the risk for dysplasia or adenocarcinoma persist in many patients. The ability of proton pump inhibitors to suppress acid profoundly and consistently may be critical in the long‐term management of Barrett’s oesophagus.
A 10‐year survey of inflammatory bowel diseases—drug therapy, costs and adverse reactions
Authors: Blomqvist P. , Feltelius N. , Löfberg R. , Ekbom A. 
Published: March 2003

Background:Drug therapy for Crohn’s disease and ulcerative colitis is based on anti‐inflammatory and immunodulating drugs, nutritional support and surgical resection. Recently, new drugs have been introduced.Aim:To report drug prescriptions, costs and adverse reactions among inflammatory bowel disease patients in Sweden between 1988 and 1997.Methods:Drug use was calculated from the national Diagnosis and therapy survey and drug costs from prescriptions and drug sales. Adverse drug reactions were obtained from the Medical Products Agency’s National Pharmacovigilance system.Results:The annual drug exposure for Crohn’s disease was 0.55 million daily doses per million population, mainly supplementation and aminosalicylic acids. Mesalazine and olsalazine had 61% within this group. For ulcerative colitis patients, drug exposure was 0.61 million daily doses per million per year and aminosalicylic acids fell from 70% to 65%. For inflammatory bowel disease patients, corticosteroids and nutritional supplementation were common. The annual average cost for inflammatory bowel disease drugs was 7.0 million US dollars. Anually, 32 adverse drug reactions were reported, mainly haematological reactions such as agranulocytosis and pancytopenia (60%), followed by skin reactions. Only two deaths were reported. Aminosalicylic acids were the most commonly reported compounds.Conclusions:Drug use for inflammatory bowel disease in the pre‐biologic agent era rested on aminosalicylic acid drugs and corticosteroids with stable levels, proportions and costs. The level of adverse drug reactions was low but haematological reactions support the monitoring of inflammatory bowel disease patients.
An evaluation of invasive and non‐invasive tests for the diagnosis of Helicobacter pylori infection in Chinese
Authors: Wong B. C. Y. , Wong W. M. , Wang W. H. , Tang V. S. Y. , Young J. , Lai K. C. , Yuen S. T , Leung S. Y. , Hu W. H. C. , Chan C. K. , Hui W. M. , Lam S. K. 
Published: March 2003

Background:Different tests are available for diagnosing Helicobacter pylori infection.Aim:To compare the most commonly used tests either alone or in combination in Chinese patients with respect to routine clinical use or research purpose.Methods:A total of 294 consecutive dyspeptic patients without previous H. pylori treatment were recruited. During upper endoscopy, biopsies were taken from the antrum and corpus, for a commercially available CLO‐test, an in‐house rapid urease test, culture, polymerase chain reaction and histological examination. Patients then received a 13C‐urea breath test. The H. pylori status of each patient was determined by a concordance of test results.Results:For routine clinical use, histology (antral plus corpus biopsies) had an accuracy of 100%, whilst the rapid urease test had an accuracy of 99.7%. The 13C‐urea breath test was equally reliable, with an accuracy of 94.5%. Combinations of two tests did not confer additional advantage over the most accurate single test. For research purposes, the accuracy of using the criteria of two positives out of three diagnostic tests was 100% and equivocal results were not found.Conclusion:Histology with or without a rapid urease test was highly accurate for routine clinical use. Alternatively, the 13C‐urea breath test was an equally reliable non‐invasive test. The two positives out of three tests approach was highly reliable in predicting H. pylori status of untreated Chinese patients in a research setting.
Evaluation of five commercial serological tests for the detection of Helicobacter pylori infection in Chinese
Authors: Szeto M. L. , Lee C. K. , Yee Y. K. , Li K. F. , Lee W. K. , Lee C. C. , Que T. L. , Wong B. C. Y. 
Published: March 2003

Background:Commercial serological tests for the detection of Helicobacter pylori infection must be locally validated. We evaluated the accuracy of five commercial tests in the Chinese population.Methods:Serum samples were collected from patients referred for upper endoscopy. Antral biopsies were taken for histological examination and culture of H. pylori. The gold standard for diagnosing H. pylori infection was positive histological staining and/or positive H. pylori culture. The serum samples were tested for H. pylori antibodies using the following tests: (i) Cobas Core Anti‐H. pylori EIA; (ii) GAP IgG; (iii) GAP IgM; (iv) H. pylori microwell EIA (Quidel); and (v) Premier H. pylori. The sensitivity, specificity and accuracy of each test was calculated according to the manufacturers’ instructions or according to a new cut‐off value.Results:A total of 158 patients were recruited amongst whom 114 (72%) were H. pylori‐positive. Indeterminate results varied from 7% to 19%. The accuracy of the tests varied from 57% to 85%. By using new cut‐off values, the accuracy was much improved, ranging from 73.4% to 86.7%.Conclusions:By defining new cut‐off values for the Chinese population, we were able to improve the performance of some of the serology tests. This illustrates the importance of local validation.
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
Authors: Sanduleanu S. , Jonkers D. , De Bruïne A. , Hameeteman W. , Stockbrügger R. W. 
Published: March 2003

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)‐1β, 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‐1β 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. pyloribacteria is a major factor in the development of atrophic gastritis during gastric acid inhibition.
Renal tubular injury is present in acute inflammatory bowel disease prior to the introduction of drug therapy
Authors: Fraser J. S. , Muller A. F. , Smith D. J. , Newman D. J. , Lamb E. J. 
Published: March 2003

Background: 5‐aminosalicylic acid (5‐ASA) has been associated with renal complications in inflammatory bowel disease. Renal function is typically monitored using serum creatinine; however, significant disease may predate increases in creatinine.Aims: To identify whether markers of early renal disease (urinary albumin, α‐1‐microglobulin [α‐1‐M] and N‐acetyl‐β‐D‐glucosaminidase [NAG], and serum cystatin C) are useful in the assessment of renal function in inflammatory bowel disease patients receiving 5‐ASA.Methods: Twenty‐one patients with a new diagnosis of inflammatory bowel disease were investigated. Samples were taken at diagnosis, and at 3‐monthly intervals after the commencement of 5‐ASA, for 1 year.Results: Mean creatinine clearance was 100 mL/min and did not change following treatment. Inflammatory bowel disease was not associated with albuminuria. Urinary N‐acetyl‐β‐D‐glucosaminidase and α‐1‐microglobulin at diagnosis were increased in 10 (48%) and 11 (52%) patients, respectively: treatment was not associated with consistent changes in urinary protein excretion. There was a significant correlation between cystatin C and creatinine clearance both at diagnosis (r=–0.533, P=0.0275) and combining the initial and follow‐up data (r=–0.601, P < 0.01), but not between creatinine and creatinine clearance (P > 0.05).Conclusions: Tubular proteinuria is an extra‐intestinal manifestation of inflammatory bowel disease irrespective of 5‐ASA treatment. Tubular proteins are not useful predictors of an adverse renal response to 5‐ASA. Serum cystatin C may be an improved marker of glomerular filtration rate in this setting.