Gastric cancer in the province of Zaragoza (Spain): a survival study.

A study of the main prognostic factors and of the overall survival rate of gastric cancer (GC) is presented. It covered 895 cases diagnosed histopathologically in the province of Zaragoza (Spain) over a ten-year period (1980-1989). The analysis of the survival rate was carried out according to the Kaplan-Meier method and the Mantel-Haenszel test. The average overall survival rate of the sample was 6.5 months and the five-year survival rate was 16.5%. Lauren's intestinal histological type is associated with a better prognosis (a five-year survival rate of 25%) than the diffuse type (15%). The survival rate with regard to gastric wall invasion ranges from 78% for T1 tumors to 8% for T4 tumors (p < 0.0001). There are significant differences in survival rate between the TNM classification stages, ranging from a five-year survival rate of 77% for Stage I to 0% for Stage IV.

Acid inhibition and long-term treatment of peptic ulcer disease.

Acid is an influencing factor in most peptic diseases, including peptic ulcers. Acid inhibition, whatever the means used to obtain it, is followed by healing of most peptic ulcers. If acid inhibition is maintained recurrences are prevented (or diminished). A quantitative correlation between the degree of acid inhibition obtained and the effectiveness of treatment has been suggested in different studies. However, it is not possible to predict in the individual subject which rate of acid inhibition is needed for healing, and which rate is needed for avoiding relapse. Acid inhibition, apart from intrinsic toxicity of the drugs used to obtain it, is not without theoretical risks, particularly bacterial overgrowth and gastric carcinogenesis. To date, these effects lack practical importance at least with the doses and durations of treatments reported. Empirical data on acid inhibition and treatment of peptic ulcers, especially duodenal ulcers, are abundant. However, pathophysiological studies are scarce. Pathophysiological data should be studied in the future in groups of patients in order to design new strategies of treatment, particularly individual treatments. Acid inhibition by drugs or surgery remains the most important treatment of peptic ulcer disease. Long-term acid inhibition by drugs is safe and effective.

[Refractory peptic ulcer: the pathogenic mechanisms]. / Ulcera péptica refractaria: mecanismos patogénicos.

The vast majority of peptic ulcers heal after treatment with either H2 receptor antagonists or omeprazole at standard doses. However, it is also recognized that a 5-10% of peptic ulcers will not heal. The possibility of identifying the factors associated with refractory ulcers would have important repercussions. Several retrospective and prospective studies have pointed out a number of clinical, environmental or intrinsic factors. In recent years 2 factors have emerged as the main cause of peptic ulcer. Helicobacter pylori infection and NSAID use, and these two factors might be involved in the pathogenesis of refractory ulcer.

[Prevalence of Helicobacter pylori in gastric pathology in Aragon]. / Prevalencia del Helicobacter pylori en patología gástrica en Aragón.

The aim of this study was to evaluate the prevalence of Helicobacter pylori in 400 patients referred for upper digestive tract endoscopy. In our area it hasn't developed yet any epidemiologic study about this disease. Helicobacter pylori was observed in 281 of the 400 patients studied (70%). No significant differences by sex were found in the subjects analyzed. There was a rise in the percentage of positivities as age increased. Helicobacter pylori were positive in 74 of the 88 patients with chronic superficial gastritis (84.1%), in 53 of the 65 with chronic atrophic gastritis (81.5%), in 16 of the 25 with chronic atrophic gastritis and intestinal metaplasia (64%), in 49 of the 63 with gastric ulcer (77.8%), in 73 of the 85 with duodenal ulcer (85.9%), in 9 of the 24 patients with gastric carcinoma (37.5%), in 5 of the 19 with stump gastritis (26.3%), where as only a few Helicobacter pylori were found in 2 of the 31 histologically normal subjects (6.5%). These findings support the wiew that Helicobacter pylori may be etiologically related to chronic gastritis and peptic ulceration, even though their precise role still remains to be determined.

[Inflammatoru bowel disease in Aragón: a more and more frequent diagnosis]. / Enfermedad inflamatoria intestinal en Aragón: un diagnóstico cada vez más frecuente.

OBJECT: To study the frequency of inflammatory bowel disease in our area. MATERIAL AND METHODS: A retrospective, hospital-based analysis identifying potential cases, with a posterior study of case records following a predefined protocol, according to international standards in diagnosis. PATIENTS: All patients with a confirmed diagnosis of Crohn's disease, ulcerative colitis, or indeterminate colitis established between 1975 and 1992 at our Hospital. RESULTS: 222 cases (ulcerative colitis: 109; Crohn's disease 93; indeterminate colitis 20) were identified and a clear trend for an increased incidence was found for the three diagnoses; with annual incidence below 1 for them all in the 1975-1977 period versus 3.66; 3.33; and 1 respectively in the 1990-1992 period. This trend was evident both for ulcerative colitis and Crohn's disease. CONCLUSIONS: The global frequency of inflammatory bowel disease has increased in the last years in Zaragoza (Spain), and its incidence in now very similar to that reported in northern European countries. Possible factors associated with this phenomenon should be pursued in future studies.

Effects of long-term treatment with lansoprazole and omeprazole on serum gastrin and the fundic mucosa.

OBJECTIVE: To compare the effects of long-term lansoprazole and omeprazole treatment (6 months) on serum gastrin levels. PATIENTS: Forty duodenal ulcer patients without previous treatment with proton pump inhibitors were randomized to receive either 20 mg/day or omeprazole or 30 mg/day of lansoprazole. Serum gastrin levels were determined on entry and every 2 months. On finalizing the study antral and fundic biopsies were obtained for immunohistochemical analysis of the enterochromaffin-like cell population. RESULTS: Before starting the treatment fasting serum gastrin was similar in both groups (108.7 +/- 60.9 pg/mL omeprazole; 102.7 +/- 56.9 pg/mL lansoprazole). The treatment with either omeprazole or lansoprazole increased serum gastrin levels, but the increase was mild, maximal at 2 months and similar between omeprazole and lansoprazole (113.44 +/- 114.9 pg/mL omeprazole vs 166.1 +/- 117.9 pg/mL lansoprazole; p > 0.05). When serum gastrin levels were individually analyzed by patient, most were below 200 pg/mL and only 3 patients (1 omeprazole/2 lansoprazole) had levels near 500 pg/mL which were not correlated with enterochromaffin-like cell hyperplasia. CONCLUSIONS: Long-term treatment with either omeprazole or lansoprazole is safe, at least during 6 months, and results in mild hypergastrinemia. No differences between these two drugs were observed.

[Comparative multicentric study of omeprazole versus ranitidine in the treatment of duodenal ulcer]. / Estudio comparativo multicéntrico de omeprazol frente a ranitidina en el tratamiento de la úlcera duodenal.

A total of 158 patients, aged 19-78 years and with endoscopically verified duodenal ulcer of at least 5 mm in maximum diameter were recruited. 79 patients were randomised to treatment with omeprazole, a proton-pump inhibitor of the parietal cell, and 79 patients were treated with ranitidine. This double blind study is the first clinical trial with omeprazole in Spain. Using "intention to treat" analysis there was no difference in healing rates at 2 weeks between the omeprazole group (70%) and the ranitidine group (59%) with p = 0.13. At four weeks, however, omeprazole healed significantly more patients (92%) than ranitidine (76%) with p = 0.005. Using per protocol analysis a similar result was obtained with no significant difference between omeprazole (71%) and ranitidine (63%) at two weeks (p = 0.3) but significantly greater healing on omeprazole at 4 weeks (97%) compared with ranitidine (83%) with p = 0.008. The influence of additional prognostic factors was assessed using a multivariate analysis. At two and four weeks, there was a significant effect of ulcer size on healing rate. At four weeks there was also a significant effect of treatment. Symptom relief was rapid in both treatments but the omeprazole group had significantly fewer days of pain and better patient's overall evaluation than ranitidine group. No serious adverse events were reported. In conclusion omeprazole healed significantly more duodenal ulcers than ranitidine and symptom relief was more rapid during omeprazole therapy.

[The debut of Crohn's disease as a gastrocolic fistula]. / Inicio de enfermedad de Crohn como fístula gastrocólica.

The case of a 66-year-old women admitted for the study of chronic diarrhea and an important deterioration in her general state is reported. Following the study undertaken the presence of a gastrocolic fistula was observed without clarifying the nature of the same thereby leading to surgical treatment. Anatomopathologic analysis confirmed the presence of a gastrocolic fistula in relation to Crohn's disease. The origin of these fistulas is usually neoplastic and the presentation as a complication of an inflammatory disease is very infrequent.

[Effect of exogenous administration of platelet-derived growth factor and epidermal growth factor on duodenal ulcer healing in rats treated with indomethacin]. / Efecto de la administración exógena de PDGF y EGF en la cicatrización de la úlcera duodenal en ratas tratadas con indometacina.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) delay peptic ulcer healing through mechanisms that are still not entirely understood. Growth factors play a significant role in healing. AIM: To evaluate whether exogenous administration of platelet-derived growth factor (PDGF) reverses the effect of indomethacin in experimental duodenal ulcers in rats and to define the potential mechanisms involved in this process. METHOD: Duodenal ulcer was induced in male Wistar rats with acetic acid. The rats were then administered indomethacin (2 mg/kg/day), PDGF-BB (30 ng/100 g/day), epidermal growth factor (EGF) (50 /kg/day) or famotidine (positive control) or the possible combinations of these. Macroscopic area, reduction in microscopic diameter, epithelial and granulation tissue proliferation, collagen secretion by granulation tissue, and gastric acid secretion were analyzed. RESULTS: Indomethacin delayed duodenal ulcer healing by decreasing cellular proliferation and inhibiting collagen secretion. PDGF and EGF accelerated healing and reversed the effects of indomethacin. The mechanisms involved were associated with an increase in collagen proliferation and secretion without affecting gastric acid secretion. Famotidine also accelerated healing and reversed the effect of indomethacin, and these effects were associated with a marked inhibition of gastric acid secretion and increase in collagen secretion by granulation tissue. CONCLUSIONS: Exogenous administration of PDGF and EGF accelerated healing and reversed the harmful effects of indomethacin in an experimental model of duodenal ulcer.