Aims-To investigate the effect of eradication of Helicobacter pylori infection on gastric epithelial damage and gastritis, scored according to the Sydney system. Methods-Gastritis scores and epithelial damage were assessed in gastric biopsy specimens before, and five weeks and one year after anti-H pylori therapy in 66 patients with H pylon related gastritis. Results-The mean initial levels of activity, inflammation, atrophy, intestinal metaplasia, and H pylon scores were higher in the antrum than in the corpus or fundus. Eradication ofHpyloni resulted in an improvement in the mean inflanumatory score in antral biopsy specimens from 2-23 before treatment to 1*32 and 1-06, respectively, five weeks and one year after treatment. Corresponding values for fundic biopsy specimens were 1*30, 036 and 0-35. Activity scores improved from 1P41 before treatment to 0-13 and zero, respectively, five weeks and one year after treatment in antral biopsy specimens and from 0-60 before treatment to zero in fundic biopsy specimens. Before treatment, epithelial damage was present in 51% of biopsy specimens taken from the antrum and 23% of those from the corpus. Five weeks after eradication of H pyloni none of the biopsy specimens revealed evidence of epithelial damage. Conclusion-Eradication ofHpylon is followed by a rapid, significant improvement in the gastritis score and resolution of epithelial damage in antral and fundic mucosa.(J7 Clin Pathol 1995;48:250-256)

The effect of ingestion of 50 g fat, 50 g protein, and 50 g starch on plasma cholecystokinin (CCK) concentrations was studied in eight healthy volunteers. Plasma CCK concentrations were measured by radioimmunoassay with Bolton-Hunter-labelled CCK 33, CCK 33 standard, and antibody T204. Antibody T204 was directed to the sulphated tyrosine region of CCK. Ingestion of fat and protein induced significant increases in plasma CCK, whereas ingestion of starch did not significantly influence plasma CCK levels. Peak increments in plasma CCK after fat (4.8 +/- 0.9 pmol/l) and protein (3.4 +/- 0.5 pmol/l) were significantly greater than that after starch (0.9 +/- 0.3 pmol/l). Similarly, the integrated plasma CCK secretion after fat (213 +/- 49 pmol/l X 120 min) and after protein (178 +/- 53 pmol/l X 120 min) was significantly greater than that found after ingestion of starch (9 +/- 23 pmol/l X 120 min). It is concluded that, in contrast to starch, fat and protein are potent stimuli for the release of CCK.

Low to moderate quality evidence indicates that EBRT reduces anal resting pressure, decreases rectal distensibility, and frequently induces telangiectasias of rectal mucosa. Objective changes may be associated with fecal incontinence, urgency, frequent bowel movements, and rectal bleeding, but these symptoms are not always related to radiation damage.

The present study was undertaken to compare the effects of equimolar amounts of long-chain triglycerides (LCT) and medium-chain triglycerides (MCT) on plasma cholecystokinin (CCK) concentrations and gallbladder contraction in man. On separate mornings and in random order six healthy volunteers ingested either 60 mmol LCT or 60 mmol MCT. Plasma CCK concentrations were measured by a sensitive and specific radioimmunoassay and gallbladder contraction by ultrasonography. Ingestion of LCT induced significant increases in plasma CCK from 2.8 +/- 0.5 to 6.5 +/- 0.7 pmol/l (p less than 0.005) and decreases in gallbladder volume from 33.4 +/- 5.9 to 13.2 +/- 4.2 cm3 (p less than 0.005). On the other hand, no significant changes in plasma CCK and gallbladder volume were found after MCT. Ingestion of MCT was followed by abdominal cramps and diarrhea, while LCT were without side effects. It is concluded that, in contrast to LCT, MCT do not induce CCK release and gallbladder contraction.