dinoprost and Duodenal-Ulcer

Topics: Anti-Ulcer Agents; Dinoprost; Duodenal Ulcer; Duodenum; Gastric Juice; Gastric Mucosa; Humans; Intestinal Mucosa; Prostaglandins; Prostaglandins E; Sucralfate

Sixty-seven adolescents suffering from duodenal ulcer (DU) were studied for the level of prostaglandins (PG) E and P2 alpha in the gastric juice and blood plasma depending on the condition of the gastric juice hydrochloric acid secretion and phase of the disease. There were no significant differences in PG content in adolescents with hyper- and normal acidity or subacidity. During the stage of aggravation PG level gets significantly increased and remains somewhat elevated during remission. We suggest that in DU adolescents there is a relative deficiency of endogenous PG that affects resistance of gastric and duodenal mucosa, which event might promote ulceration even with normal secretion of gastric juice. These considerations should be taken account of in conducting a therapy.

Topics: Adolescent; Chronic Disease; Dinoprost; Duodenal Ulcer; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Humans; Male; Prostaglandins E

Radioimmunoassay was used to determine prostaglandin (PGE-2) and cyclic nucleotides (cAMP and cGMP) concentrations in the serum before, 1 and 2 hours after standard test breakfast (5066 kJ) in 65 patients with duodenal ulcer. Basal hyperproduction of prostaglandins and cyclic nucleotides were interpreted as an adaptation-compensatory mechanism. The unbalance of their aftermeal reactions persistent even in ulcer healing may belong to factors of the disease progression.

Topics: Adaptation, Biological; Adult; Biopsy; Cyclic AMP; Cyclic GMP; Dinoprost; Dinoprostone; Duodenal Ulcer; Endoscopy, Digestive System; Humans; Male; Middle Aged; Radioimmunoassay

A clinico-morphological study was made of processes in the gastro-duodenal mucosa during treatment of duodenal ulcer by de-nol. Results indicate that the dyspeptic and pain syndrome disappeared after de-nol treatment within 4-7 days in 78.3% of patients, the ulcer scarred in the course of 21.4 days. Advantages of de-nol treatment are shown electron-microscopically, by studying biopsy specimens of the mucosa before and after treatment.

Topics: Anti-Ulcer Agents; Biopsy; Dinoprost; Drug Evaluation; Duodenal Ulcer; Duodenum; Humans; Intestinal Mucosa; Microscopy, Electron; Organometallic Compounds; Prostaglandins E; Time Factors

We measured gastric and duodenal mucosal prostaglandin concentrations in 69 patients with active or inactive duodenal or gastric ulcer disease and 26 non-ulcer controls. Each underwent endoscopy enabling us to obtain multiple biopsies from the gastric body and antrum and from the duodenal bulb and postbulbar duodenum for measurement of mucosal prostaglandin concentrations, as well as a single biopsy from each region for mucosal histology. Using a multivariate linear regression model, we found that neither gastric nor duodenal ulcer disease significantly affected gastric or duodenal mucosal prostaglandin concentrations. Mucosal prostaglandin concentrations were similar at the edge of the ulcer and in the adjacent non-ulcerated mucosa. Neither gender symptoms, smoking, use of H2-receptor antagonists, disease activity, nor Helicobacter pylori infection had an independent effect on mucosal prostaglandins in any region. Gastritis in the body of the stomach was associated with significantly higher prostaglandins, while older age was associated with significantly lower gastric and duodenal prostaglandins. Gastroduodenal mucosal prostaglandins are thus not altered in patients with active or inactive peptic ulcer disease, even when multiple demographic and histologic variables are taken into consideration.

Topics: Age Factors; Dinoprost; Dinoprostone; Duodenal Ulcer; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metaplasia; Middle Aged; Prevalence; Prospective Studies; Stomach Ulcer

The amount of prostaglandins (PD) E, F2 alpha and I2 (measured as 6-keto-Pg F1 alpha) in endoscopic biopsy specimens of gastric corpus' mucosa also as the concentration of Pg E and F2 in gastric juice of cirrhotic patients without or with gastric and duodenal ulcer were measured by radioimmunoassay. Release of Pgs with gastric juice (in the basal state and after histamine stimulation) was also significantly less in these patients. It was concluded that the severe disturbance of endogenous biosynthesis Pgs in gastroduodenal mucus of cirrhotic patients may play an important role in the development of ulcer disease in these patients.

Topics: Biopsy; Chronic Disease; Dinoprost; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Humans; Liver Cirrhosis; Peptic Ulcer; Prostaglandins; Prostaglandins E; Radioimmunoassay; Stomach Ulcer

In the present study we evaluated the contents of endogenous prostaglandins type E2 and F2 alpha in the antral mucosa, and the type E2 in the duodenal mucosa in a group of thirty non-ulcer dyspeptics in comparison with a group of thirty duodenal ulcer patients. A significantly reduced concentration of duodenal and antral PGE2 was found in ulcer patients as compared with dyspeptic subjects. A significantly increased concentration of antral PGE2 was observed in cases with active superficial antral gastritis, either in dyspeptics or in duodenal ulcer patients, as compared with normal antrum cases. A significantly increased level of PGF2 alpha was found in active superficial gastritis of the dyspeptic group.

Topics: Adult; Dinoprost; Dinoprostone; Duodenal Ulcer; Duodenum; Dyspepsia; Female; Gastric Acid; Humans; Intestinal Mucosa; Male; Middle Aged; Pyloric Antrum

Topics: Adolescent; Adult; Dinoprost; Duodenal Ulcer; Duodenum; Female; Humans; Intestinal Mucosa; Male; Middle Aged; Nucleotides, Cyclic; Prostaglandins E; Prostaglandins F

Synthesis of prostaglandins (PGE2, PGI2 and PGF2 alpha) and thromboxane A2 was investigated in short term incubates of duodenal mucosa biopsies. Mucosa close to the ulcer site synthesised significantly less PGF2 alpha (p less than 0.001) and PGI2 (p less than 0.002) measured as its stable metabolite 6-oxo-PGF1 alpha than healthy mucosa from non-ulcer patients. In paired biopsies taken from the ulcer site and opposite the ulcer in the same patient PGF2 alpha and PGI2 syntheses were both significantly and similarly depressed when compared with normal mucosa. Synthesis of PGE2 and TxA2 (as its stable metabolite TxB2) was not different in any tissue. There is a defect in the ability of the human duodenal mucosa in duodenal ulcer disease to synthesise PGF2 alpha and PGI2; the defect is not limited to the ulcer site.

Topics: Dinoprost; Dinoprostone; Duodenal Ulcer; Duodenum; Epoprostenol; Humans; Intestinal Mucosa; Prostaglandins; Prostaglandins E; Prostaglandins F; Thromboxane A2

Most of the experiments have verified the cytoprotective effect of prostaglandins on the gastric mucosa and only few observations are known to deal with "cytoprotection" exerted on the duodenal or intestinal mucosa. Duodenal ulcers were produced by cysteamine (CEA). The treatment with different prostaglandins (PGI2, PGF2 alpha, PGE2) was carried out every six hours during the 48-hour experimental period. The obtained results indicate that neither prostacyclin nor prostaglandin-F2 alpha has any significant effect on CEA-induced duodenal ulceration, while prostaglandin-E2 exerts a slight anti-ulcerogenic effect. It is possible that cytoprotection is not the result of the same process in the duodenal and gastric mucosa: alternatively, three prostaglandins are not involved in the pathomechanism of CEA-induced duodenal ulceration.

Topics: Animals; Cysteamine; Dinoprost; Dinoprostone; Duodenal Ulcer; Epoprostenol; Female; Intestinal Mucosa; Prostaglandins; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains