Background-Bile acid toxicity has been shown in the gastric, colonic, and hepatic tissues; the eVect on oesophageal mucosa is less well known. Aims-To determine the spectrum of bile acids refluxing in patients with gastrooesophageal reflux disease and its relation to oesophageal pH using a new technique of combined oesophageal aspiration and pH monitoring. Methods-Ten asymptomatic subjects and 30 patients with symptoms of gastrooesophageal reflux disease (minimal mucosal injury, erosive oesophagitis (grade 2 or 3 Savary-Miller), Barrett's oesophagus/stricture; n=10 in each group) underwent 15 hour continuous oesophageal aspiration with simultaneous pH monitoring. Bile acid assay of the oesophageal samples was performed using modified high performance liquid chromatography. Results-The peak bile acid concentration and DeMeester acid scores were significantly higher in the patients with oesophagitis (median bile acid concentration 124 µmol/l; acid score 20.2) and Barrett's oesophagus/stricture (181 µmol/l; 43.3) than patients with minimal injury (14 µmol/l; 12.5) or controls (0 µmol/l; 11.1). The predominant bile acids detected were cholic, taurocholic, and glycocholic acids but there was a significantly greater proportion of secondary bile acids, deoxycholic and taurodeoxycholic acids, in patients with erosive oesophagitis and Barrett's oesophagus/stricture. Although bile acid reflux episodes occurred at variable pH, a temporal relation existed between reflux of taurine conjugates and oesophageal acid exposure (r=0.58, p=0.009). Conclusion-Toxic secondary bile acid fractions have been detected in patients with extensive mucosal damage. Mixed reflux is more harmful than acid reflux alone with possible toxic synergism existing between the taurine conjugates and acid. (Gut 1999;44:598-602)

Results support important between-group differences with diagnostic and therapeutic implications. asds often present atypically in children with seizures. However, both groups showed widely varying social and linguistic presentations.

Ten type 1 diabetic patients recorded their daily home blood glucose values, pre- and post-prandially, for 12 weeks. Blood was collected weekly for HbA1c and total haemoglobin measurement. A rolling 28-day mean of all blood glucose values and a glycation index (the ratio of the HbA1c to the rolling mean blood glucose) were calculated. In the pooled patients' data, there was a large scatter of results about the HbA1c versus mean blood glucose regression line. There was less variation in the results of individual patients. The glycation indices showed marked inter-individual variation, and in 60% of patients there was an inverse relationship between glycation index and mean blood glucose, suggesting a non-linear relationship between mean blood glucose and HbA1c. Patients should be monitored on the basis of their own previous results, and in some patients blood HbA1c may be a less sensitive index of mean blood glucose concentration at higher glucose levels.

The use of plasma lactate to assess metabolic or circulatory impairment requires definition of critical preanalytical and analytical parameters. Stability has been documented for only 15 min after acquisition when samples were collected with fluoride and transported on ice. We examined time elapsed before analysis, storage temperature, and the antiglycolytic agent used to define preanalytical conditions. Plasma lactate was measured with a Kodak Ektachem 700XR analyzer. In controlled studies on volunteers, storage on ice slowed but did not eliminate the production of lactate; for samples collected with sodium fluoride (F) and potassium oxalate (OX), lactate increased by 0.2 mmol/L after 1 h, then changed little regardless of the storage temperature. For patients' samples collected in F/OX, the mean increase was only 0.15 mmol/L after 24 h. Samples with leukocytosis (neutrophil counts 23 x 10(9)-52 x 10(9)/L) were also stable, with a mean increase of 0.3 mmol/L at 8 h. Use of the antiglycolytic agents F and OX (at 60 and 12 mmol/L, respectively) maintained apparently stable lactate concentrations at room temperature for up to 8 h without special handling.