Esophageal cast: a manifestation of graft-versus-host disease.

Diffuse involvement of the gastrointestinal tract by graft-versus-host disease (GVHD) is a common complication of bone marrow transplantation. The esophageal involvement in this disease tends to be a vesiculobullous, ulcerative or desquamative process. To our knowledge, esophageal cast has not been described in the context of GVHD. However, it has been described as a result of trauma to the esophagus or in association with bullous disease of the skin. We present a case of esophageal cast in a patient with chronic GVHD following bone marrow transplant.

Small-intestinal mucosal protein synthesis and whole-body protein turnover in alcoholic liver disease.

We used stable-isotope-labelled amino acids to measure the effects of alcoholic liver disease (ALD) on whole-body protein turnover and small-intestinal mucosal protein synthesis. Groups comprising eight patients with ALD and eight healthy control subjects were studied. They received primed, continuous intravenous infusions of L-[1-(13)C]leucine after an overnight fast; after 4 h, duodenal biopsies were obtained via endoscopy. Protein synthesis was calculated from protein labelling relative to intracellular leucine enrichment. Rates of duodenal mucosal protein synthesis were 2. 58+/-0.32%.h(-1) (mean+/-S.D.) in the normal subjects and 2.04+/-0. 18%.h(-1) in the ALD patients (P<0.003), despite the fact that the protein synthetic capacity (microgram of RNA/mg of protein) was higher in ALD patients (160+/-14 compared with 137+/-6 microgram/mg; P<0.003). The mucosal cell size (protein/DNA ratio) was lower in ALD patients (9.23+/-0.91 compared with 13+/-2.2 microgram/mg; P<0.002). Although the mean rates of whole-body protein turnover were not significantly different between the two groups (204+/-18 and 196+/-44 micromol leucine.h(-1).kg(-1) for ALD and control subjects respectively), there was, in the ALD patients, an inverse relationship between the rate of small-intestinal mucosal protein synthesis and the severity of ALD; furthermore, there was a direct relationship between the rate of whole-body protein turnover and the severity of ALD. Thus there was an inverse relationship between the rate of small-intestinal mucosal protein synthesis and the rate of whole-body protein turnover in ALD patients, which was not seen in the normal subjects.

Rates of small intestinal mucosal protein synthesis in human jejunum and ileum.

We investigated possible differences in the rates of mucosal protein synthesis between the proximal and distal regions of the small intestine. We took advantage of access to the gut mucosa available in otherwise healthy patients with ileostomy in whom the terminal ileum was histologically normal. All subjects received primed, continuous intravenous infusions of L-[1-(13)C]leucine after an overnight fast. After 4 h of tracer infusion, jejunal biopsies were obtained using a Crosby-Kugler capsule introduced orally; ileal biopsies were obtained via endoscopy via the ileostomy. Protein synthesis was calculated from protein labeling relative to intracellular leucine enrichment obtained by appropriate mass spectrometric measurements. Rates of jejunal and ileal mucosal protein synthesis were significantly different (P < 0.001) at 2.14 +/- 0.2 and 1.2 +/- 0.2 %/h (means +/- SD). These are lower than rates in normal healthy duodenum (2.53 +/- 0.25 %/h), suggesting a gradation of rates of synthesis along the bowel. Together with other data, these results suggest that mucosae of the bowel contribute not more than 10% to whole body protein turnover.

Effect of omeprazole therapy on the survival of Helicobacter pylori, urease activity, and antral gastric histology in patients with duodenal ulcer.

BACKGROUND: Helicobacter pylori is associated with chronic active gastritis and peptic ulceration (PU). Omeprazole is a proton pump inhibitor that is effective in healing PU and reducing gastritis. Previously it has been found that omeprazole has some bacteriostatic activity against H. pylori both in vitro and in vivo and in inhibiting urease activity in vitro. Our aim was to evaluate the effect of omeprazole on H. pylori colonization of the gastric mucosa, urease activity in vivo, and the presence of associated gastritis in patients with duodenal ulcer (DU). MATERIALS AND METHODS: We studied 12 patients (7 men and 5 women, ages 22-68 yr) with Du larger than 5 mm in diameter with a positive CLOtest (Delta West Ltd., Australia). Omeprazole, 20 mg bid, was given for 8 weeks to each patient, patients were endoscoped at the end of this period to check for healing of DU, and repeat biopsies were obtained from the gastric antrum for histological analysis, CLOtest, and culture. RESULTS: DU healed completely in all patients. Likewise in all patients there was significant reduction in the urease activity, from 22.1 +/- 4.17 to 1.58 +/- 0.92 units/ml (p < .001; 95% confidence interval of the difference between means, 32.7-14.1), and reduced H. pylori density, from 1,403.46 +/- 128.23 to 422.5 +/- 172.39 colony-forming units (CFU) per milligram of tissue biopsy (p < .001; 95% confidence interval of the difference between means, 1,486.1-590.5). The numbers of H. pylori were reduced on the gastric mucosa after omeprazole therapy and disappeared in six patients, a result that correlated with a negative CLOtest reading after 24 hours. CONCLUSION: Omeprazole, 20 mg bid, is capable of reducing H. pylori numbers and urease activity in vivo. There was no significant reduction in the severity of antral gastritis in DU patients studied.

Increased rates of duodenal mucosal protein synthesis in vivo in patients with untreated coelia disease.

BACKGROUND AND AIMS: A robust, reproducible method for the measurement of protein synthesis in the gastrointestinal mucosa was applied to investigate possible differences between the rate of duodenal mucosal protein synthesis in coeliac patients and normal control subjects. PATIENTS AND METHODS: Eight patients, means (SD) (51 (10) years, 57 (11) kg, 160 (6) cm) with newly diagnosed untreated coeliac disease and seven control subjects (48 (11) years, 71.5 (12) kg, 172 (10) cm) received primed, continuous, intragastric (IG) and intravenous (i.v.) infusions of L-[1-13C]leucine and L-[1-13C]valine after an overnight fast. Distal duodenal biopsy specimens were obtained at endoscopy performed after 240 minutes of infusion. Protein synthesis was calculated from protein labelling relative to intracellular free amino acid enrichment, after appropriate mass spectrometric measurements. RESULTS: Rates of duodenal protein synthesis were significantly greater in coeliac patients than in control subjects (i.v. tracer, coeliac v control, 3.58 (0.45) v 2.26 (0.22)%/h, p< 0.05; IG tracer, 6.25 (0.97) v 2.34 (0.52)%/h respectively, p < 0.01). The rates of mucosal protein synthesis calculated on the basis of the tracer infused via the intragastric route were higher in patients with coeliac disease than in control subjects. Tissue protein/DNA ratios were significantly reduced in coeliac patients (coeliac v control, 9.2 (1.6) mg/micrograms v 13.0 (2.2) mg/micrograms respectively, p < 0.05) suggesting smaller mucosal cell size in coeliac patients. CONCLUSIONS: Despite the villous atrophy and reduced cell size observed in coeliac disease, the rates of mucosal protein synthesis are considerably increased. These results suggest that a high rate of protein synthesis may be adaptive to a high rate of protein breakdown or mucosal cell loss in coeliac patients.

Gut mucosal protein synthesis measured using intravenous and intragastric delivery of stable tracer amino acids.

We measured the rates of mucosal protein synthesis during the simultaneous delivery of [1-13C]leucine and [1-13C]valine delivered either intragastrically or intravenously to investigate any influence of the route of supply of the tracers. Dependent on the route, there were marked differences in the gradient of labeling between the plasma and intramucosal leucine and valine; i.e., for intravenous tracers the ratio was 1.73 +/- 0.16, but for intragastric tracers it was 0.65 +/- 0.12 (P < 0.05). Incorporation of intravenous tracer into mucosal protein was linear with time, and irrespective of tracer route, the calculated fractional rates of protein synthesis were identical when based on the intracellular labeling of the leucine or valine tracer, i.e., with intravenous 2.58 +/- 0.32%/h and with intragastric 2.45 +/- 0.36%/h. The results demonstrate that a robust and reproducible method of measurement of gastrointestinal mucosal protein synthesis has been developed and that use of either intragastric or intravenous routes of tracer administration gives comparable results. The high rates measured suggest that the gastrointestinal mucosa contributes substantially to whole body protein synthesis in normal healthy subjects.

Is Asacol as effective as sulphasalazine in maintaining remission of Crohn's disease and ulcerative colitis?

To compare the efficacy of Asacol (mesalazine coated with Eudraget-S) as a maintenance therapy with that of sulphasalazine, relapse rates of patients with ulcerative colitis and Crohn's disease, treated with sulphasalazine or Asacol were assessed in a retrospective study. A total of 164 patients were investigated, 127 on sulphasalazine and 37 on Asacol. None of the patients on Asacol was changed from sulphasalazine because of lack of efficacy to sulphasalazine. Relapse rates were measured over a 4 year period. In ulcerative colitis these were sulphasalazine 10/77 (13.0%), Asacol 5/20 (25.0%), NS; in all Crohn's disease patients, sulphasalazine 12/50 (24.0%), Asacol 11/17 (64.7%); P less than 0.0025. In patients with Crohn's disease with ileal involvement, relapse rates were sulphasalazine 9/28 (32.1%), Asacol 9/11 (81.6%), P less than 0.0125; without ileal involvement, sulphasalazine 3/22 (13.6%), Asacol 2/6 (33.4%), NS. This study suggests that Asacol is as effective as sulphasalazine in maintaining remission in ulcerative colitis and in patients with Crohn's disease without ileal involvement. Sulphasalazine seems to be more effective than Asacol in maintaining remission in patients with Crohn's disease with terminal ileal involvement.

Spiral shaped microorganisms in the human duodenal mucosa.

A new spiral shaped microorganism, Gastrospirillum hominis, distinct from Helicobacter pylori, has recently been described in the gastric mucosa. We report a patient with duodenal erosions who was found to have these organisms in his duodenal mucosa. This bacterium is not necessarily specific to the stomach, and its association with peptic damage needs to be studied further.