Nocturnal gastric acidity pattern in gastro-oesophageal reflux disease with or without oesophagitis.

The reasons why few patients with gastro-oesophageal reflux disease develop oesophagitis are not yet clear. One of the factors whose role is still debatable is the gastric acid secretory state. The aim of this study was to evaluate whether differences exist in nocturnal gastric acidity between patients with oesophagitis and refluxers without oesophageal lesions. We studied 65 patients with gastro-oesophageal reflux disease, 37 of whom presented erosive oesophagitis, while 28 had no oesophageal lesions. Thirty-one healthy volunteers were used as controls. In both patients and controls intragastric and intraoesophageal pH were measured continuously using 2 in-dwelling glass electrodes, placed in the gastric corpus and in the oesophagus. Mean intragastric pH was calculated over 3 nocturnal time periods: 11.00 p.m.-07.00 a.m.; 11.00 p.m.-03.00 a.m.; 03.00 a.m.-07.00 a.m. Patients with oesophagitis had a lower nocturnal gastric pH (1.6 +/- 0.2) than either refluxers without oesophagitis (2.2 +/- 0.3) (p = 0.05) or controls (2.6 +/- 0.4) (p = 0.02). The difference occurred entirely in the second part of the night. Furthermore, in the same time period, oesophagitis sufferers had a higher percentage of oesophageal acid exposure at pH < 2 (0.7 +/- 0.2) than refluxers without oesophagitis (0.2 +/- 0.1) (p = 0.05), suggesting that gastric findings are of pathogenetic relevance. Patients with reflux oesophagitis have a higher nocturnal intragastric acidity than refluxers without oesophagitis. This difference, confined to the second half of the night, may be due to an altered circadian pattern of gastric acid secretion and may partially explain why only some refluxers develop oesophagitis.

DNA flow cytometric evaluation of cell cycle distribution in ulcerative colitis: a proposed method for assessing severity of disease.

The assessment of disease severity in ulcerative colitis depends mainly on subjective variables, and an objective method of assessing mucosal inflammation is needed. Determination of the synthetic phase of the cell cycle is an accurate expression of inflammatory activity in the colonic mucosa. The aim of the study was to find out if the proliferative index or the synthetic phase (S phase) of the colonic mucosa of patients with ulcerative colitis, as evaluated by DNA flow cytometry, is a reliable and reproducible marker of disease activity. Sixty consecutive patients with ulcerative colitis of different degrees of activity were entered into the study and submitted to colonoscopy plus multiple rectal biopsies. Disease severity was defined for each patient by means of a clinical, endoscopic, and histological score. Flow cytometry was used to calculate the proliferative index and the S phase of the cell cycle. A statistically significant correlation (p < 0.001) was found between all indices of severity. It is suggested that flow cytometric evaluation of the cell cycle in the rectal mucosa may be an efficient method of assessing severity of disease and efficacy of medical treatment in ulcerative colitis.

Effect of short- and long-term treatment with omeprazole on cell cycle distribution in the gastric mucosa. Results of a flow cytometric study.

Omeprazole may exert an effect on gastric mucosal proliferation by inhibiting gastric acid secretion and increasing serum gastrin levels. It may also influence the kinetics of endocrine cells and the oxyntic mucosa. The aim of the present study was to evaluate the cell cycle in different gastric compartments following short- (1 month) and long-term (6 months) administration of two different dosages of omeprazole by means of a flow cytometric method. We also determined serum gastrin levels at the same time. No differences in cell cycle distribution of the antrum, body, and fundus were found in the two different dosage groups after 1 month of therapy, considering the synthetic phase (S-phase) of the cell cycle. A statistically significant increase in S-phase was reported after long-term therapy in the mucosa of the fundus and body of the stomach in both groups. Gastrin levels showed no clear correlation with cell cycle distribution variables. We postulate a proliferative adaptation of the oxyntic mucosa to long-term drug administration not mediated by gastrin influence.