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At least 55 records · Page 3Linked to original sources
PubMed1990

Human antral damage induced by alcohol is potentiated by enprostil.

Enprostil, a synthetic analogue of prostaglandin E2, has been shown to protect the human gastroduodenal mucosa from aspirin injury. This study was designed to determine if enprostil protected against alcohol damage. A double-blind, randomized, cross-over study was performed on eight healthy adult men. After an overnight fast, a gastroscope was inserted and the antral mucosa was sprayed with a 10-mL test solution containing either enprostil (70 micrograms) or its vehicle (control). After 15 minutes, mucosal injury was scored (0-5), and the mucosa was sprayed with 100 mL 80% ethanol. Mucosal injury was scored after a further 15, 20, 25, and 30 minutes. The entire experiment was recorded on video film, which a second endoscopist used to score the damage independently. The two experiments were separated by an interval of 1 week. There was close agreement between the two endoscopists (r = 0.9385), and their scores were averaged. Using Friedman's two-way analysis of variance, a highly significant (P less than 0.00004) increase in injury was demonstrated following enprostil pretreatment. The Wilcoxin signed rank test showed the differences to be significant (P less than 0.05) at every time point. We conclude that enprostil, rather than protecting the human antral mucosa from alcohol injury, appears to potentiate this injury and may itself be damaging in therapeutic concentrations. This unexpected result cannot yet be explained but demands caution in the clinical use of enprostil.

Adult↗
PubMed1986

Reduction by enprostil of aspirin-induced blood loss from human gastric mucosa.

Enprostil's ability to protect human gastric mucosa against aspirin-induced damage was investigated in a controlled study. Damage was assessed as blood loss into gastric washings measured spectrophotometrically using orthotolidine in the presence of hydrogen peroxide. Phenol red was used to correct for recovery rates. Five doses of aspirin, 600 mg, given over 48 hours increased blood loss ninefold compared with placebo. Administration of enprostil 35 micrograms twenty minutes before each dose of aspirin halved this blood loss. After enprostil administration, the pH of both aspirated gastric juice and washings was significantly elevated, suggesting that an antisecretory dose had been used. Increased losses of phenol red occurred following both aspirin and enprostil administration, suggesting enhanced gastric emptying or possible absorption of phenol red as a result of aspirin damage. Side effects related mainly to the alimentary system were associated with enprostil treatment. Enprostil reduced aspirin-induced mucosal blood loss but the mechanism is unclear.

Adult↗
PubMed1986

Treatment of duodenal ulcer with enprostil, a prostaglandin E2 analogue.

Enprostil is a synthetic prostaglandin E2 analogue with gastric anti-secretory, cytoprotective, and gastrin lowering properties. The current multi-center, double-blind, placebo-controlled study was undertaken to evaluate the efficacy and safety of enprostil (35 micrograms twice daily) for the treatment of duodenal ulcers. The study enrolled 87 patients between the ages of 18 and 85 with an endoscopically proved duodenal ulcer between 0.5 and 3.0 cm in its longest dimension and with no other serious medical conditions or abnormal laboratory tests results. Treatment groups were comparable in age, sex, smoking status, ulcer history, and baseline ulcer size. The results indicated that the healing rate for enprostil at two weeks was 38 percent, compared with a placebo rate of 23 percent (p = 0.151). At four weeks, 70 percent of the enprostil-treated patients had healed ulcers, compared with 49 percent of the placebo-treated patients, a statistically significant difference (p = 0.048). Although within the enprostil group the healing rate was higher in nonsmokers (86 percent) than in smokers (58 percent), this difference did not reach statistical significance. Side effects included diarrhea (14 percent) and headache (7 percent). These results indicate that 35 micrograms of enprostil twice daily provides effective and safe therapy for patients with duodenal ulcer.

Adolescent↗
PubMed1997

Effect of enprostil on omeprazole-induced hypergastrinemia and inhibition of gastric acid secretion in peptic ulcer patients.

This study was performed to examine the effects of additional enprostil administration on hypergastrinemia and gastric acid suppression induced by omeprazole. Serum gastrin concentrations were measured in 10 peptic ulcer patients (six Helicobacter pylori-positive and four Helicobacter pylori-negative patients) before treatment, after two weeks of omeprazole (20 mg/day), and after two weeks of omeprazole and enprostil (50 micrograms/day). The additional acid inhibitory effect of enprostil was evaluated by 24-hr intragastric pH measurements in five healthy Helicobacter pylori-negative volunteers. After omeprazole treatment, the serum gastrin level of Helicobacter pylori-positive patients (3.5-fold of control) was markedly higher than that of Helicobacter pylori-negative patients (1.7-fold of control). Additional treatment with enprostil suppressed serum gastrin levels to 0.4-fold and 0.7-fold of omeprazole treatment levels in Helicobacter pylori-positive and Helicobacter pylori-negative patients, respectively. In healthy volunteers, median pH recorded during the nonmeal daytime interval increased significantly with additional enprostil. Thus, enprostil reduces undesirable omeprazole-induced hypergastrinemia, especially in Helicobacter pylori-positive patients, and effectively suppresses acid secretion.

Adult↗
PubMed2000

Enprostil, a prostaglandin-E(2) analogue, inhibits interleukin-8 production of human colonic epithelial cell lines.

We previously reported that intracolonic administration of enprostil, a prostaglandin-E(2) (PGE(2)) analogue, had therapeutic effects on acute colitis induced in rodents by dextran sulfate sodium (DSS). In addition, production of growth-regulated gene product/cytokine-induced neutrophil chemoattractant-1 [GRO/CINC-1; an interleukin(IL)-8 like cytokine] was suppressed in the inflamed tissues. In the present study we used a human colon cancer cell line (HT-29) to investigate enprostil effects on the IL-8 production of intestinal epithelial cells stimulated by various stimulants. In a MTT assay, concentrations of enprostil >10(-5)M had cytotoxitic effects on HT-29 cells. Furthermore, 10(-6) M enprostil suppressed IL-8 production in HT-29 cells, SW620 and CaCo2 stimulated with interleukin-1 beta (IL-1 beta) or lipopolysaccharide (LPS), but did not suppress this response when cells were stimulated with tumour necrosis factor (TNF)-alpha. These results suggest that enprostil affects a point in the pathway between the IL-1 receptor or LPS receptor and nuclear factor-kappa B(NF-kappa B), without affecting the pathway between the TNF receptor and NF-kappa B, with the latter factor being required for the IL-8 gene transcription. The therapeutic effect of exogenous enprostil on DSS colitis may involve the inhibition of IL-8 production in colonic epithelial cells stimulated by IL-1 beta or LPS.

Colitis, Ulcerative↗
PubMed1989

Central and peripheral effects of prostaglandin E2 and enprostil on exocrine pancreatic secretion in rats.

Prostaglandin E2 (PGE2) has been reported to exert some centrally mediated effects on intestinal motility and secretion and on gastric secretion, but it is not known whether such central effects exist on pancreatic secretion. The central and peripheral effects of PGE2 and enprostil, a long-acting, potent PGE2 analogue, were studied in conscious and anesthetized rats fitted with pancreatic fistulae. In chronically implanted, conscious rats, PGE2 inhibited the secretion of fluid, bicarbonate, and total protein in the pancreatic juice, both after i.v. or intracerebroventricular (icv) injections. The maximal inhibition was similar after both injection procedures (about 45% for fluid and bicarbonate and 60% for protein), but the potency of PGE2 was three to 10 times greater by the icv than the i.v. route. Enprostil also inhibited pancreatic secretion in a dose-related way. The maximal inhibition was larger than after PGE2 injection (about 70% for fluid and bicarbonate and 90% for protein). The potency of enprostil was five to 10 times lower by the icv than by the i.v. route. The diversion of gastric secretion suppressed the effect of icv PGE2 on fluid and bicarbonate output but not on protein and did not change the effect of enprostil on all the variables of pancreatic secretion. Adrenergic antagonists did not suppress the effect of icv PGE2 or enprostil on pancreatic secretion. In anesthetized rats, i.v. PGE2 inhibited hormone-stimulated protein secretion but did not change fluid and bicarbonate output, while i.v. enprostil inhibited cholecystokinin-stimulated fluid, bicarbonate, and protein output in the pancreatic juice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of enprostil on basal and meal-stimulated gastric acid and pepsin secretion, serum gastrin and gastric emptying in healthy persons.

Ten healthy volunteers took part in a double-blind, randomized, cross-over study of the effect of single doses of enprostil (70 micrograms) and placebo on basal and meal-stimulated gastric acid, pepsin secretion and serum gastrin. Meal-stimulation was induced by modified sham feeding combined with repeated gastric instillation and withdrawal of meat soup. When studied between 1 and 2.5 hours after oral administration of the drug, enprostil decreased basal acid output by 92% (P less than 0.001) and stimulated acid output by 70% (P less than 0.001). Basal and stimulated volumes of gastric juice were decreased by 50% (P less than 0.02) and 35% (P less than 0.002), respectively. Enprostil decreased stimulated pepsin output by 34% (P less than 0.05), but had no effect on the concentration of pepsin. Neither basal nor stimulated serum gastrin concentrations were affected by enprostil. Percent recovery of the meal was measured by an unabsorbable marker, polyethylene glycol, instilled into the stomach mixed with the soup. Polyethylene glycol recovery decreased from 89% with placebo to 67% with enprostil (P less than 0.01), indicating an enhanced gastric emptying rate with enprostil.

Adult↗
PubMed1990

The effect of enprostil on duodeno-jejunal motility in man.

Motor changes could be involved in the pathogenesis of diarrhoea that complicates the treatment of ulcer disease by prostaglandins. Our aim was to assess the effect of enprostil, a synthetic analogue of PGE2, on duodeno-jejunal motility. During this randomized double-blind crossover study, two manometric recordings, each lasting 20 h (12.00-08.00 hours), were carried out during dosing with 35 micrograms enprostil b.d. or placebo (eight volunteers: part 1), or during dosing with 35 or 70 micrograms enprostil b.d. (nine volunteers: part 2). Subjects were only allowed a standard dinner at 18.00 hours. During fasting, in part 1, the number of phase 3 activity patterns (PIIIs) was higher with enprostil than with placebo (P less than 0.01), without any difference in their characteristics; the overall duration of phase 1 activity was longer with enprostil than with placebo (P less than 0.01). In part 2, during fasting the number and characteristics of the PIIIs were not different, but there was a dose-related increase in PI, and decrease in PII activity. Fed motor patterns did not differ between the two doses of enprostil.

Adult↗
PubMed1990

A comparison between enprostil and ranitidine in the management of gastric ulceration.

In a randomly allocated, double-blind, endoscopically controlled study, 98 patients with gastric ulcers were treated with either (a synthetic prostaglandin of E2-like structure) enprostil 70 micrograms b.d. or 150 mg ranitidine b.d. The healing rates at 4, 8 and 12 weeks were enprostil 57, 91 and 94% and for ranitidine 55, 88 and 98%, respectively. Following ulcer healing, half the patients were followed for 1 year without treatment and the others were given 70 micrograms enprostil nocte. Endoscopy was repeated in both groups after 6 and 12 months or if dyspeptic symptoms returned. The recurrence rate without maintenance at 6 and 12 months, following ranitidine therapy, was 67 and 75%, and after enprostil therapy 50 and 61%, respectively. On maintenance enprostil, the recurrence rates were 28 and 40%. Forty-seven per cent of patients who completed maintenance treatment had a proven ulcer recurrence within 6 months of stopping therapy. Diarrhoea was a common side-effect of enprostil therapy. Seven patients were withdrawn because of diarrhoea or abdominal pain.

Double-Blind Method↗
PubMed1987

Enprostil and ranitidine: comparative efficacy and safety in patients with duodenal ulcer.

This randomised, double-blind, double-dummy, multiclinic study of duodenal ulcer healing compared the efficacy and safety of enprostil with ranitidine. The six week trial admitted 164 patients with endoscopically demonstrated duodenal ulcer. Ratings of symptoms and adverse events were collated from patients' daily diaries, and endoscopy was repeated to verify healing after four weeks and, if appropriate, after six weeks. Medication used was enprostil (35 micrograms capsule) or ranitidine hydrochloride (150 mg tablet) with matching placebos twice daily. After six weeks, 81% of patients treated with enprostil and 95% of those treated with ranitidine had healed ulcers, a statistically significant difference (p = 0.007). There were no differences between treatment groups for the number of days until the daytime ulcer pain completely ceased. Night-time ulcer pain ceased significantly earlier in the group receiving ranitidine (p = 0.019) and was less severe during the week before the last visit (p = 0.001); daytime pain for ranitidine users was also less severe (p = 0.020) during this week. Mild to moderate adverse experiences were reported by 44% of enprostil and 35% of ranitidine patients. There were no severe adverse events. In conclusion, both enprostil and ranitidine were found to be safe and effective in the treatment of duodenal ulcer. However, the ranitidine regimen used in this trial produced better results than the enprostil regimen.

Clinical Trials as Topic↗
PubMed1989

[Efficacy and tolerability of enprostil in the treatment of duodenal ulcer. Comparison with cimetidine].

Enprostil, a synthetic PGE2, has been shown to have an inhibitory effect on gastric acid secretion, a mucoprotective effect and a postprandial lowering effect on gastrin. A double blind randomized study was performed in 80 patients, in order to evaluate the efficacy and safety enprostil (35 mu b.i.d) as compared to cimetidine (400 mg b.i.d) in duodenal ulcer. Healing rates after two, four and six weeks of treatment, as based on endoscopic evaluation, were 35, 72 and 83 p. 100 for enprostil and 45, 73 and 83 p. 100 for cimetidine, respectively. There were no significant differences between treatment groups. The time to relief of nighttime and daytime ulcer pain and antacid consumption were similar in the two groups. The patient's overall subjective assessment was better in the cimetidine group, but this was not confirmed by physicians' opinions. Diarrhea was observed in 7 p. 100 of patients treated by enprostil compared with 5 p. 100 for patients treated by cimetidine. One enprostil treated patient withdrew from the trial prematurely because of abdominal pain. This study demonstrates the efficacy and safety of enprostil in the treatment of active duodenal ulcer at the dosage of 35 micrograms twice daily.

Adult↗
PubMed1989

Effect of oral enprostil, a synthetic prostaglandin E2, on intestinal brush border membrane lipid composition following abdominal irradiation in the rat.

Previous studies have demonstrated that external abdominal irradiation alters intestinal nutrient transport and brush border membrane (BBM) phospholipid content. This study was undertaken to assess the possible protective effect of oral dosing of enprostil, a synthetic E2 prostaglandin, on the BBM marker enzyme and lipid composition of non-irradiated control (CONT) animals and of rats exposed seven days perviously to a single dose of 600 cGy external abdominal irradiation (RAD). Half the CONT and RAD animals were orally dosed with enprostil 5 mcg/kg body weight, two and one mornings before the day of irradiation, and one hour before 600 cGy; the remaining half were dosed with placebo according to the same schedule. BBM were isolated and purified from the animals seven days post-irradiation for analysis of marker enzymes and lipid composition. Radiation was associated with a decline in jejunal and ileal BBM activity of sucrase. Enprostil was associated with a decline in the ratio of alkaline phosphatase/sucrase in jejunal BBM from irradiated rats, despite its preventing a radiation-associated decline in BBM sucrase activity. Radiation was associated with changes in ileal BBM phospholipids, and these alterations were not prevented with enprostil. Furthermore, enprostil given to non-radiated control rats altered BBM composition, such as increased jejunal and ileal lysophosphatidylethanolamine, and lowered ileal BBM sphingomyelin and phosphatidylethanolamine. Thus, enprostil failed to protect the intestine from the effects of abdominal irradiation on BBM phospholipids, but did partially prevent the effect of abdominal irradiation on jejunal sucrase activity.

Abdomen↗
PubMed1986

Synergistic interaction between an H2-receptor antagonist and enprostil on 24-hour intragastric pH, serum gastrin concentration, and tissue immunoperoxidase staining for gastrin, somatostatin, and serotonin in a patient with metastatic gastrinoma.

A 56-year-old woman newly diagnosed as having Zollinger-Ellison syndrome due to a metastatic gastrinoma underwent 24-hour intragastric pH monitoring, serum gastrin (total, G-17 and G-34) measurements, and immunoperoxidase staining of duodenal, antral, and gastric body biopsies for gastrin, somatostatin, and serotonin. Determinations were made while the patient was given different doses of ranitidine, enprostil (a synthetic orally administered prostaglandin E2), or ranitidine plus enprostil. Following are the findings from this single-patient study: Intragastric pH was persistently low but varied in response to food when the patient was given ranitidine. Immunocytochemical staining of antral biopsies obtained before the patient was treated revealed a reduced number of cells containing G-17 and G-34 but an increase in the antral somatostatin-containing D-cells. Treatment with 35 micrograms of enprostil BID plus 300 mg of ranitidine BID for two and 11 weeks was associated with an increased number of duodenal G-cells, a decrease in antral D-cells, and a decrease in the number of antral serotonin-containing cells. Enprostil in a dosage of 35 or 70 micrograms BID had no effect on intragastric pH, but when enprostil was given in combination with ranitidine, postprandial and nocturnal intragastric alkalinity was accentuated along with a return of duodenal and antral G-cells and a loss of the antral D-cell hyperplasia. Optimal pH control was achieved with 300 mg of ranitidine BID; more frequent dosing with ranitidine did not further increase intragastric pH. Both the total serum gastrin concentration and G-17 levels fluctuated in response to meals. The serum concentrations of total gastrin, G-17, and G-34 were reduced with enprostil and with ranitidine.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

Gastric antisecretory and antiulcer properties of enprostil, (+/-)-11 alpha, 15 alpha-dihydroxy-16-phenoxy-17,18,19,20-tetranor-9-oxoprosta- 4,5,13(t)-trienoic acid methyl ester.

Prostaglandins of the E series have been shown, both in animals and humans to produce gastrointestinal antisecretory and antiulcer effects. Enprostil, a modified allenic prostaglandin E was found to be a highly potent inhibitor of gastric HCl secretion in a variety of species. In rats, in which both the pylorus and esophagus were ligated, p.o. ED50 values and 95% CL for inhibiting acid secretion evoked by histamine, pentagastrin and carbachol were 9.9 (6.7-15), 40 (11-145) and 0.83 (0.78-0.89) micrograms/kg, respectively. In inhibiting histamine-evoked acid secretion, enprostil was more potent when administered p.o. than when injected into the duodenum or s.c. When enprostil was injected directly into the pouch of Heidenhein dogs, intense antisecretory activity occurred, ED50 = 0.9 (0.7-1.1) micrograms/kg, whereas, when given p.o. to the main stomach the ED50 was 6.6 (3.2-13.6) micrograms/kg. Administration of cimetidine either p.o. or to the pouch resulted in virtually identical ED50 values, viz., 2.9 and 3.1 mg/kg. Enprostil also inhibited dimaprit- and pentagastrin-induced acid secretion in cats with permanent gastric fistulae. The oral ED50 values for inhibiting acid secretion evoked by these two secretagogues were 2.5 (1.4-4.3) and 0.8 (0.5-1.5) micrograms/kg, respectively. Enprostil was extremely potent in preventing indomethacin plus "cold stress" ulcers in rats. When given orally the ED50 was 0.61 (0.31-1.22) and s.c. it was 22 (9.0-52) micrograms/kg. It was also highly potent in preventing cysteamine-induced duodenal ulcers when given p.o., ED50 = 20 (17-23) micrograms/kg. Thus, enprostil is a highly potent antisecretory and antiulcer agent. It appears to act topically; directly at gastric mucosal sites.

Animals↗
PubMed1993

Effects of proglumide and enprostil on omeprazole-induced fundic endocrine cell hyperplasia in rats.

Long-term treatment with omeprazole induces hyperplasia of enterochromaffin-like cells, closely related to hypergastrinemia. We studied whether proglumide, an antagonist of gastrin/CCK receptor, and enprostil, a synthetic prostaglandin E2 derivative, might inhibit this hyperplasia. Six groups of 8 rats were treated for 10 weeks: a) untreated controls; b) omeprazole 10 mumol/kg; c) proglumide 500 mg/kg; d) enprostil 30 micrograms/kg; e) association of omeprazole and proglumide; f) association of omeprazole and enprostil. Serum gastrin levels were measured at different times during treatment. After sacrifice, fundic argyrophil cells were assessed by Grimelius' staining. Serum gastrin levels and argyrophil cell density were not modified in proglumide- and enprostil-treated groups, as compared with controls. Omeprazole increased significantly these two parameters. When given with omeprazole, proglumide decreased significantly serum gastrin levels and argyrophil cell density, as compared to omeprazole alone, while enprostil did not modify significantly these two parameters. These results indicate that proglumide, but not enprostil, can counteract the omeprazole-induced argyrophil cell hyperplasia in rats.

Animals↗
PubMed1989

Inhibitory action of enprostil (4,5-dehydro-16-phenoxy-17,18,19,20-tetranor-PGE2) on tetra-gastrin stimulated acid secretion in human subjects.

A double-blind study was conducted to examine the effect of enprostil on tetra-gastrin stimulated gastric acid secretion in twelve healthy male volunteers. Each subject underwent four tests in random order on separate days with oral doses of 15, 25, 35 micrograms enprostil and placebo. After measuring basal secretion and gastrin release, tetra-gastrin was injected intramuscularly. Gastric secretion and gastrin release were measured over the next two hours. Enprostil dose-dependently inhibited tetragastrin stimulated gastric secretion volume, acid and pepsin output. There were significant differences in gastric acid secretion inhibition between the 15 and 25 micrograms doses, and the 15 and 35 micrograms doses, but only a slight dose response was seen between the 25 and 35 micrograms doses with no significant difference. Serum gastrin level was not influenced by the administration of enprostil. No side effects attributed to enprostil were observed throughout the study.

Adult↗
PubMed1988

Reduction of serum lipoproteins in man by the oral administration of a prostaglandin analogue (enprostil).

Retrospective analysis of ulcer healing trials utilizing enprostil, a synthetic dehydroprostaglandin E2 analogue, has demonstrated a 10% or greater reduction in total serum cholesterol in 64%, 64% and 67%, respectively, of hypercholesterolemic subjects receiving the drug in doses of 70 micrograms, 35 micrograms, and 7 micrograms bid, respectively. Only 16% of subjects receiving placebo exhibited a similar reduction (P less than 0.05). The median percent changes for hypercholesterolemic patients receiving enprostil 70 micrograms, 35 micrograms, or 7 micrograms bid, and placebo were -17%, -13%, -11%, respectively, while the median percent change for those on placebo was 0% (P less than 0.05). Eight normocholesterolemic subjects participated in a double-blind crossover study comparing enprostil 70 micrograms/d with its placebo. Nine days of enprostil administration was associated with reductions in total serum cholesterol (-16%) and apolipoprotein B (-16%) and with significant reductions from baseline for LDL-cholesterol (-22%), the LDL/HDL-cholesterol ratio (-13%), and the ratio of serum apolipoprotein B to apolipoprotein A-1 (-12%). Relative to placebo, mean HDL-cholesterol, total triglycerides, and apolipoprotein A-1 concentrations remained unchanged. Daily oral administration of microgram quantities of enprostil is associated with reductions in total cholesterol, LDL-cholesterol, and apolipoprotein B suggesting therapeutic potential of this synthetic prostaglandin for the treatment of hyperlipidemia.

Administration, Oral↗
PubMed1989

Suppression of alimentary lipemia in man by a prostaglandin analogue (enprostil).

Oral administration of Gardrin (enprostil), a synthetic prostaglandin E2 structural analogue, is associated with a rapid reduction in serum lipoproteins as well as a reduction in meal-stimulated increments for glucose, insulin, and glucose-dependent insulinotropic peptide (GIP). The latter effects appear to be related to be a reduction in carbohydrate absorption. To test the effects of enprostil on an oral fat challenge, 6 healthy males received in random order 35 micrograms enprostil (enp) and placebo (pla), each as a single dose. Thirty minutes following study drug, subjects consumed an 856 kcal test meal with 76 g total fat (80%), 29 g carbohydrate (14%), and 14 g protein (6%). Compared with placebo, enprostil resulted in significant or near significant reductions in insulin, total triglycerides (TG), chylomicron TGs, and GIP while glucose was modestly elevated. The integrated areas under the insulin, GIP, TG, and chylomicron curves were reduced by 59% for insulin and greater than 90% for the remainder, respectively. Thus a single dose of enprostil appears to decrease alimentary lipemia through an effect on chylomicron formation and/or clearance. Other effects, such as a delay in gastric emptying, may be contributory. These observations may have potential therapeutic applications, and additional studies are ongoing to define mechanisms.

Administration, Oral↗