April 1995
• CELL PROLIFERATION IN THE GASTROINTESTINAL EPITHELIUM OF PATIENTS WITH DUODENAL ULCER AND HELICOBACTER PYLORI INFECTION. P~Tracz, S. Gustavsson, A. Uribe. Dept of Surgery, Viister~ts Hospital, Dept of Surgery, University Hospital, Uppsala and Dept of Medicine, Karolinska Institute, Danderyd Hospital, Stockholm, Sweden Helicobacter pylori (HP) infection is of major importance for the development of peptic ulcer. A role for HP in gastric cancer has also been suggested. From a cell kinetic Viewpoint, ulcerations may occur when cell proliferation is inhibited and/or when cell losses to the lumen cannot be compensated by changes in the crypt cell production rate. Our principal aim was to examine the mitotic activity in duodenal crypts of patients with active duodenal ulcer, before and after eradication of HP. Methods. 23 patients (average age 58 years) with duodenal ulcer and HP infection as demonstrated by culture of gastric antral biopsies were treated with Amoxicillin (2 gr daily) and omeprazol (20 mg x 2) for 2 weeks. Upper gastrointestinal endoscopy was performed at the beginning of the study and after 2 months. In addition to antral biopsies for culture and histological evaluation, 2 biopsy specimens from duodenum were taken at day 1 and 60 and fixed in Carnoy. Twenty duodenal crypts and 20 antral glands were isolated using the microdissection technique and the total number of mitotic figures present in the whole crypt was counted in a light microscope. Biopsy specimens from 13 subjects with dyspeptic symptoms, normal endoscopic findings and negative urease test were used as controls. Results. Helicobacter pylori was eradicated in 9/23 patients as shown by the gastric antral cultures and histological sections. A median 4.05 (2.26-5.53) mitoses/crypt was observed at the beginning of the study which was not significantly different from 4.75 (2.72-7.16) mitoses/crypt observed after eradication of HP. The median of controls was 5.15 (4.23-5.46) mitoses/crypt (n.s). In the antral mucosa, the median number of mitoses per gland was 3.2 (1.76-4.15) at day 1 which was not different from 3.15 (1.61-4.67) observed after eradication of HP. Interestingly, 7/9 patients had still histological evidence of antral gastritis at the end of the study. Conclusion. Helicobacter pylori does not primarily affect cell proliferation in the human gastroduodenal mucosa. Our results suggest that the perviously reported increased DNA synthesis in the antral mucosa of these patients may be a cell kinetic phenomenon inherent to gastritis instead of a direct action of HP on proliferating cells.
CHRONIC GASTRITIS AND NON ULCER DYSPEPSIA IN ELDERLY PATIENTS Q,Triossi, I.Tampieri, G.Michieltti, M.Ricci Maccarini, E.Bertinelli, T.Casetti. Servizio di Gastroenterologia, Ospedale S. Maria delte Croci, Ravenna, Italy Chronic gastritis (CG) is a very common condition both in young and ederly people. Both patients (pts) who complaint dyspeptic symptoms and asymptomatic subjects show chronic inflammation of gastric mucosa. It never has been demonstrated a correlation between dyspeptic symptoms and chronic gastritis. Aim of our study was to evaluate the relation between CG and dyspeptic symptoms in elderly pts. Since 01.01.1992 to 31.12.1992, 874 pts > 70 years old with epigastric pain or disconfort were submitted to gastroscopy. Patients with gastroesophageal reflux, irritable bowel syndrome, previous major abdominal surgery, peptic ulcer or erosions, systemic or organic diseases, were escluded from the study. We selected 193 pts with nonulcer dyspepsia (NUD) (98 M, mean age 79 yrs; 95 F, mean age 79 yrs). A second group of 47 asymptomatic subjects (CS) (25M, mean age 79 yrs; 22F mean age 78 yrs) who performed gastroscopy for positivity of hemmoccult test, served as control. In each pts and CS were performed 2 antral biopsy to evaluate inflammatory infiltration of antral mucosa. Moreover we analized the histologic (Giemsa) presence of helicobacter pylori. Our results were analized by statistic test of x 2. RESULTS: We found CG in 186 pts with NUD (96 %) and in 24 CS (51%) (X2 =66,86; p < 0 . 0 0 1 ) . . W e found the helicobacter pylori in 147 out of 186 pts (79%) with CG and in 19 out of 24 CS (79 %) with CG; we didn't find helicobacter pylori in 7 pts (4%) with normal antral mucosa. CONCLUSIONS: Chronic gastritis is more frequent in pts with non ulcer dyspepsia than in asymptomaic subjects. In according with international Letterature our results suggest that helicobacter pylori is often associated with chronic gastritis in erderly patients.
Esophageal, Gastric, and Duodenal Disorders
A243
ACUTE NON VARICEAL UPPER GASTROINTESTINAL BLEEDING: ENDOSCOPIC INJECTION THERAPY O.Triossi, I.Tampieri, G.Michieletti, M.Ricci Maccarini, E.Bertinelli, T. Casetti. Servizio di Gastroenterologia Osp. S. Maria delle Croci. Ravenna. Italy Recently, endoscopic injection therapy has been currently employied for acute gastrintestinal (GI) bleeding treatment. Since 1988 we used saline solution (7.1% NaCt) plus epinefrine (1/10.000) as suggested by Hirao M. & Kobayashi T. (Gastrointest. Endosc 1985; 31:313) We injected 2ml of solution into each quadrant of the edge of the lesion and then we injected directly around or into the bleeding or nonbleeding visible vessel. Usually the range of the solution volume injected was 10-16 to 20-26 ml. Since 01.01.1998 to 12.31.1993 we performed 760 emergency endoscopies for suposed acute upper GI bleeding; 159 patient were selected for injection therapy. Forrest classification and site of lesions are reported in the table. n:
SITE
81: 57: 14: 07:
Duodenum Stomach Anastomosis Esophagus
Forrest classification (51%) (36%) (09%) (04%)
lalb2 a2b-
21 (13 %) 67 (42 %) 56 (35%) 15.(10 %)
RESULTS: Immediate haemostasis was obtained in all patients, 142 out of 159 (89%) did not present relapses; 17 patients presented a second bleeding: in 12 of 17 a second treatment was effective, 2 patients underlain to surgery and 3 died for massive bleeding. The overall mortality of patients was 8.7% while bleeding relatedmortality was 1.9% (3 patients). No local or systemic complication due to injection therapy was observed. Our patients usually complain for epigastrie pain lasting 5 to 20 minutes. CONCLUSION: Our data suggest that injection of hypertonic saline solution plus epiuefrine is effective and safe for acute non-variceal upper GI hemorrhage treament.
THE CYTOPROTECTIVE EFFECTS OF ZINC SULPHATE ON CYSTEAMINE-INDUCED DUODENAL ULCER IN THE RAT. B. Troskoh V. Simicevic, M. Dodig I. Rotkvie, M. Duvnjak, T. Brkic, M. Banie. Dept. of Gastroenterolo~, Clinical Hospital ~Sestre Milosrdnice", Zagreb, Croatia. Exogeniously administered zinc compounds have been shown to have antiulcer activity in the development of gastric lesions. The aim of this study was, therefore, to evaluate the effects of zinc sulphate (ZnSO4) pretreatment in a model of duodenal ulcer induced by cysteamine. Fifty adult female Wistar rats, 180 - 250 gr. b.w., were divided into five groups. Three groups recieved a single oral dose of ZnSO4 in the following doses: 20, 40 and 80 mg/kg b.w., while the fourth group served as a control and reeieved an equivolume of saline orally. All of these animals recieved cystcamine subcutaneously in a dose of 400 mg per kg b.w. one hour following the pretreatment regimen. The fifth group reeieved a single oral application ofZnSO 4 in a dose of 80 mg/kg, without eys~amine, in order to determine absorption. Animals were saerifised 24h following cysteamine application and duodenal lesions were assessed. Blood and tissue samples were also taken and zinc concentrations were determined using atomic absorption spectrophotometry. Duodenal ulcers developed in 80°.6 of the control animals, that were not pretrcated with ZnSO 4. No lesions were noted in the group of animals that reeieved ZnSO 4 in the dose of 80 mg/kg. In the group of ammals that were treated with ZnSO 4 in the dose of 40 mg/kg. 50% of the antmals developed duodenal ulcers. In the lowest dose group (20 mg/kg b.w), duodenal ulcers developed in the same percentage as the control group. The serum zinc concentration in the animals pretreated with 80 mg/kg ZnSO4, but did not recieve cysteamina, was significantly higher than the group treated with the same dose and cysteamine application. There is also a significant difference in the zinc serum concentration of the largest dose when compared to the remaining groups. No statistical significance was noted in the tissue concentrations of the ZnSO4 and cysteamine treated animals. In conclusion, the results of this study indicate a protective role of zinc in the onset of duodenal lesions. This protection is dose-dep~dsnt. Serum fine conomtrations are significantly higher in groups in which duodenal ulcers did not occur, but there is no positive correlation with expected higher tissue concentrations in ulcer-developed groups according to some previous findings of endogenous zinc activity.