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PubMed1992

Two weeks of oral synthetic E2 prostaglandin (Enprostil) improves the intestinal morphological but not the absorptive response in the rat to abdominal irradiation.

Enprostil, a synthetic E2 prostaglandin, was administered in a dose of 5 micrograms/kg body weight by gastric tube to rats for 14 days following abdominal irradiation with a single dose of 600 cGy from a 137Cs source. Enprostil prevented the body weight loss and the reduced food intake observed in irradiated animals given placebo, and also prevented the irradiation-associated decline in the mucosal weight and surface area of the ileum. Enprostil given to nonirradiated animals reduced the maximal transport rate (Vmax) and the apparent Michaelis constant (Km*) for the ileal uptake of D-glucose, but did not prevent the irradiation-associated decline in the ileal uptake of glucose. Thus, there is a dissociation of the effects of Enprostil on the morphological and the absorptive properties of the intestine. It is concluded that a 2-week course of a daily oral dose of E2 prostaglandin begun shortly after a single exposure to nonlethal abdominal irradiation prevents the radiation-associated reduction in the intestinal mucosal surface area and the animal's body weight, but does not prevent the malabsorption of glucose.

Animals↗
PubMed1990

No abortion-inducing effect of the ulcer-healing dose of the synthetic prostaglandin E2 analogue enprostil in first trimester.

Milligram-range doses of E2 prostaglandins have long been used to induce labor or abortion in the second and third trimesters of pregnancy. Enprostil, a synthetic dehydroprostaglandin E2 structural analogue, is administered in microgram doses for the treatment of acute duodenal ulcer and acute gastric ulcer. This study examined the effect of the ulcer-healing dose and twice the ulcer-healing dose upon women in the first trimester of pregnancy. Two hundred and seven women who had requested legal abortion in the first trimester participated in two randomized, double-blind, placebo-controlled, parallel studies. They received two doses of enprostil 35 micrograms (the recommended dose for the treatment of duodenal and gastric ulcer) (n = 51), 70 micrograms (twice the recommended dose) (n = 53), or placebo (n = 103) 12 h apart. No drug-induced abortions occurred in any of the first-trimester pregnancies. Vaginal bleeding occurred in 4% of volunteers receiving the lower dose and 4% receiving the higher dose of enprostil. Vaginal bleeding occurred in up to 2% of volunteers on placebo. Although not recommended for pregnant women, if enprostil is given inadvertently to pregnant women with ulcers, it is unlikely to endanger the pregnancy during the first trimester.

Abortifacient Agents↗
PubMed1987

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

The safety and efficacy of enprostil, 35 micrograms twice daily, and of cimetidine, 400 mg twice daily, in the treatment of duodenal ulcers were compared in a randomized, double-blind, parallel, multiclinic study. Endoscopy was performed before treatment and at 2-week intervals for 6 weeks or until the ulcer healed. Patients recorded their drug compliance, antacid use, ulcer symptoms, and adverse experiences daily. One hundred and six patients entered the trial, of which 104 were eligible for the initial endoscopy analysis. Base-line characteristics were similar in the two treatment groups. The cumulative healing rates in the enprostil group were 56%, 86%, and 92% at 2, 4, and 6 weeks, respectively, and those in the cimetidine group were 53%, 84%, and 90% (NS). The healing rates for nonsmokers at 6 weeks were 96% in the enprostil group and 97% in the cimetidine group, which were significantly greater than those for smokers--88% and 81%, respectively. There were no significant differences in the duration, severity, or frequency of daytime or nighttime pain between the groups. Seventeen of the enprostil patients (32%) reported 21 adverse experiences during the trial, and 20 of the cimetidine patients (39%) reported 23 adverse experiences. No patients withdrew because of adverse experiences. The two drugs were similarly safe and effective in the treatment of duodenal ulcer.

Adolescent↗
PubMed1988

Prostaglandins and CCl4-induced liver cell mortality. The effect of the prostaglandin analogue enprostil.

Prostaglandins have been reported to reduce the carbon tetrachloride (CCl4)-induced liver cell injury in rats. The object of the present experiments was to examine the effect of the prostaglandin E2 analogue enprostil on the survival of isolated liver cells exposed to CCl4. Liver parenchymal cells were isolated from rat livers by collagenase perfusion and released into a 'suspension' buffer. Aliquots of the cell suspension were incubated with 1 micrograms or 0.5 microgram CCl4, and to parallel test suspensions 20 ng enprostil was added 5-10 min before CCl4. Incubation was performed on ice, at room temperature, and at 37 degrees C. The average percentage of dead cells after CCl4 treatment was significantly reduced by pretreatment with enprostil at room temperature (1 microgram CCl4: 69 +/- 21% and 44 +/- 13%, respectively) and after 10 min of incubation at 37 degrees C (1 microgram Cl4: 56 +/- 25% and 37 +/- 27%; 0.5 microgram CCl4: 51 +/- 33% and 29 +/- 18%, respectively). When the liver cell mortality approximated 100% after long-term incubation at 37 degrees C, no protective effect of enprostil was observed.

Animals↗
PubMed1995

Enprostil impairs cholesterol and fat absorption.

BACKGROUND: Enprostil, a synthetic dehydroprostaglandin E2 structural analogue primarily developed for treatment of gastritis, has been shown also to lower serum cholesterol. METHODS: We studied cholesterol metabolism in seven hypercholesterolemic subjects before, during, and after a low-dose enprostil (18 micrograms/day) treatment, measuring serum lipids, cholesterol absorption by an oral double-isotope method, fecal cholesterol elimination by the balance technique, and fecal fat. In addition, an oral fat load test with vitamin A was performed. RESULTS: The drug treatment reduced serum concentrations of total and low-density lipoprotein (LDL) cholesterol by 8.2% and 7.9% (p < 0.05), respectively, and cholesterol absorption efficiency by 18% (p < 0.05), and increased fecal output of neutral sterols by 20% (p < 0.05), bile acids by 24% (NS), and cholesterol synthesis by 30% (p < 0.05). Postabsorptive concentrations of triglycerides and vitamin A in chylomicrons were reduced 3-4 h after the intake of the test meal. Fecal fat excretion was doubled during the enprostil treatment. CONCLUSIONS: Enprostil reduces serum cholesterol concentrations, apparently by inhibiting cholesterol absorption so that fecal cholesterol elimination is increased in association with a mild fat malabsorption. Enhanced intestinal motility may contribute to these changes, frequently causing abdominal fullness or mild pain without diarrhea.

Adult↗
PubMedDate not supplied

Combination of enprostil and cimetidine is more effective than cimetidine alone in treating gastric ulcer: prospective multicenter randomized controlled trial.

BACKGROUND/AIMS: Little is known about the clinical efficacy of co-therapy of enprostil, a prostaglandin E2 analogue, with a histamine H2-receptor antagonist. We aimed to assess the additive benefit of enprostil in combination with cimetidine for treating gastric ulcer in a prospective multicenter randomized controlled trial. METHODOLOGY: In 43 hospitals 171 intention-to-treat (ITT) patients, diagnosed as having gastric ulcer by endoscopy, were randomly allocated to receive either enprostil 25microg b.i.d. and cimetidine 400mg b.i.d. (Group E=85), or cimetidine 400mg b.i.d. alone (Group C=86) for 8 weeks. Healing was examined by endoscopy at 4 and 8 weeks. RESULTS: Per protocol (PP) analysis comprised 166 patients (E=82, C=84). Despite no significant advantage at 4 weeks (E=55.3%, C=42.2%), the combination yielded higher healing rates at 8 weeks by ITT (E=89.4%, C=68.6%; p<0.001) and PP analysis (E=92.7%, C=70.2%; p<0.001). Symptom relief rates [E, C] at 2, 4, and 8 weeks were [80.2%, 68.3%] (not significant), [97.4%, 88.3%] (p<0.05), and [95.6%, 87.0%] (p<0.05), respectively. Significant advantage was observed in the patients aged 40 or older, with solitary ulcer (>5mm in diameter), and without smoking or drinking habits. No adverse effects were critical. CONCLUSIONS: Enprostil safely and significantly augmented gastric ulcer healing and symptom relief by cimetidine.

Adult↗
PubMed1987

Enprostil reduces G-cell hyperplasia and hypergastrinemia in duodenal ulcer.

A 42-year-old man with a 26-year history of duodenal ulcer volunteered for a 24-hour intragastric pH monitoring study, at which time his fasting gastrin concentration was found to be elevated. Secretin injection decreased the serum gastrin concentration. When not on treatment his total gastrin, gastrin-17 (G-17), and gastrin-34 (G-34) response to a protein-containing breakfast was marked. Immunocytochemical staining of antral biopsies showed hyperplasia of gastrin-containing cells, more pronounced for G-17 than for G-34. Cimetidine or cimetidine plus pirenzepine increased 24-hour intragastric pH, whereas pirenzepine alone rendered the gastric contents more acidic, particularly overnight. The total serum gastrin concentrations increased after meals and were unaffected by cimetidine or pirenzepine; enprostil, however, reduced the postprandial increase in total gastrin, G-34, and G-17. After six weeks of treatment with enprostil, the number of cells containing G-17 and G-34 was reduced. The findings show that G-cell hyperplasia may occur in the presence of a normal fasting serum gastrin concentration; fasting serum gastrin concentrations may fluctuate widely over time; the food-stimulated increase in G-17 was greater than that for G-34, and is associated with more pronounced antral hyperplasia for G-17 and G-34; and enprostil blunts the postprandial increase in G-17, G-34, and total gastrin. These observations suggest that enprostil may reduce G-cell hyperplasia and hypergastrinemia.

Adult↗
PubMed1991

[Comparative effects of diazepam, ranitidine , sodium citrate and enprostil on pH and gastric volume in preanesthetic medication].

A study was designed to assess the efficacy of oral premedication with diazepam or enprostil in preventing the gastric aspiration syndrome in fasted patients scheduled for elective surgery, and to compare the results with those obtained with ranitidine and sodium citrate. The study included 120 consecutive patients undergoing urological or plastic surgery, randomly assigned to four groups of 30. Two hours before anaesthesia, the patients from three groups were given, with 30 ml of water, either 10 mg diazepam, or 150 mg ranitidine, or 35 micrograms enprostil. Those in the fourth group were given 30 ml of 0.5 M sodium citrate, ten minutes before induction. Anaesthesia consisted in the administration of thiopentone, fentanyl, vecuronium and nitrous oxide in oxygen. After endotracheal intubation, a gastric tube was inserted. The stomach fluid content was completely aspirated, and then again 60 and 120 min after induction, as well as at the end of surgery. Age, weight and duration of surgery were comparable in the four groups. Mean pH in the diazepam group was much lower than that in the other groups, both just after induction (2.3 +/- 1.54; p less than 0.001 vs. ranitidine and sodium citrate; p less than 0.01 vs. enprostil) and at the end of surgery (3.2 +/- 2.03; p less than 0.01 vs. ranitidine and sodium citrate; p less than 0.05 vs. enprostil). There was more than 0.4 ml.kg-1 gastric juice in the sodium citrate group.(ABSTRACT TRUNCATED AT 250 WORDS)

Antacids↗
PubMed1990

The effect of the E2 prostaglandin enprostil, and the somatostatin analogue SMS 201 995, on the growth of a human gastric cell line, MKN45G.

The effect of enprostil and the somatostatin analogue SMS 201 995 on the growth of a clonal variant of the human gastric adenocarcinoma cell line, MKN45, was studied. The derived cell line grew twice as fast as MKN45 when grown as a xenograft line in nude mice. However, it did not respond trophically to gastrin either in vitro or in vivo (unlike MKN45) although it possessed the same number of gastrin receptors as the parental line. Gastrin production by the cell line during in vitro culture was twice that of MKN45; thus, the cell line was denoted MKN45G. When MKN45G was grown as xenografts in nude mice (n = 10/group), enprostil (20 micrograms/kg/day) significantly inhibited tumour growth when administered continuously by an osmotic mini-pump from day 1 to day 7 of a 20-day experiment, and induced tumour regression when administered from day 7 to day 14. Enprostil reduced postprandial serum gastrin levels when administered from day 7 to day 14 and prevented gastrin release by MKN45 in vitro. SMS 201 995 at doses of 25 and 240 micrograms/kg/day induced tumour regression when administered from day 1 to day 7 and the former dose reduced post-prandial serum gastrin levels at day 5. Gastrin release by MKN45G was not affected by SMS 201 995 in vitro, thus its effect may not be mediated directly via gastrin, requiring interaction between other hormones or growth factors in the in vivo situation.

Adenocarcinoma↗
PubMed1995

Weakness of mucosal barrier in portal hypertensive gastropathy of alcoholic cirrhosis. Effects of propranolol and enprostil.

BACKGROUND/AIMS: It has been suggested that the vulnerability of gastric mucosa is increased in patients with cirrhosis as a result of a PGE2 deficiency. Therefore, we evaluated whether PGE2 mucosal generation, and gastric potential difference - a reflection of the gastric mucosal barrier - were correlated to endoscopic features and whether these alterations could be alleviated. METHODS: The potential difference was measured before (basal) and after a stimulation test by aspirin. The serum levels of gastrin and glucagon were also determined. Finally, the effects of a 1-week administration of propranolol or enprostil were tested on potential difference. The endoscopic grade of portal hypertensive gastropathy was assessed according to McCormack et al. The results are presented respectively for controls, patients with mild gastropathy, and patients with severe gastropathy. Comparisons were made using variance or covariance analysis after adjustment with age. RESULTS: Basal potential difference was significantly different between the three groups: -30.6, -28.8, -24.9 mV, p <0.05, respectively. The effects of aspirin administration on potential difference parameters were significantly different between the three groups (irritability index: 35 +/- 25, 92 +/- 98, 114 +/- 74 mV2.min, p <0.05, respectively) when non-responders to aspirin were excluded. PGE2 mucosal generation was significantly increased in both the antrum (9.8, 19.5, 19.7 ng/mg proteins, p<0.05, respectively) and in the corpus (8.1, 14.0, 20.2 ng/mg proteins, p<0.05, respectively). PGE2 generation was not related to potential difference. Glucagon serum levels were related to the grade of gastropathy. A 1-week administration of 160 mg/d long-acting propranolol, 35 micro g/d enprostil or placebo did not significantly modify basal potential difference. CONCLUSIONS: Portal hypertensive gastropathy is characterized by a decreased potential difference proportional to the endoscopic severity. The gastric mucosa of patients with cirrhosis seems to be more susceptible to aspirin than that of healthy subjects. It appears that the role of PGE2 is controversial in portal hypertensive gastropathy. Propranolol and enprostil do not improve this decreased potential difference.

Adrenergic beta-Antagonists↗
PubMed1986

Protective effects of the synthetic prostaglandin enprostil on the gastric microvasculature after ethanol injury in the rat.

The effect of pretreatment with the synthetic prostaglandin E2 analogue enprostil on ethanol damage to the rat gastric mucosa was studied. Microvascular casts were prepared and studied by scanning electron microscopy. The permeability of mucosal capillaries to fluorescein isothiocyanate-labeled albumin (FITC-albumin) given intravenously was examined by fluorescence microscopy. After administration of ethanol (1 ml absolute ethanol intragastrically) alone, casts showed gross disruption of the normal structure, with large foci of loss of the patency of the capillary network, frequently extending to the level of the submucosal vessels. There was exudation of casting material into the mucosal interstitium and onto the surface of the cast. After administration of FITC-albumin, there was a marked increase in interstitial fluorescence throughout the full thickness of the mucosa. Pretreatment with enprostil (1 microgram/kg intragastrically) prevented most of the damaging effects of ethanol. Increased microvascular permeability to FITC-albumin was noted only in the most superficial layers of the mucosa. These studies characterize the effect of ethanol on the gastric microvasculature and indicate that pretreatment with enprostil restricts this damaging effect to the superficial mucosal microvessels. These studies further suggest that microvascular damage is an early event in ethanol injury, apparently preceding epithelial erosion.

Animals↗
PubMed1986

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

Enprostil is a synthetic prostaglandin E2 analogue developed by Syntex. In a randomized, double-blind trial involving 128 patients with duodenal ulcer disease, four weeks of treatment with enprostil at doses of 70 micrograms twice daily and 35 micrograms twice daily produced healing rates (78 percent and 65 percent, respectively) that were statistically significantly higher than the placebo rate (39 percent; p less than 0.05). In a subgroup of smokers, ulcer healing occurred with statistically significantly greater frequency at both the high dose (70 percent) and the low dose (60 percent) when compared with the rate in the placebo group (32 percent; p less than 0.05). The only clinically important side effect was diarrhea, which was generally mild, self-limited, and of short duration. This study demonstrated that enprostil is highly effective in the treatment of duodenal ulcer and has a favorable safety profile.

Adolescent↗
PubMed1986

Comparison of enprostil and cimetidine in active duodenal ulcer disease. Summary of pooled European studies.

Data were combined for statistical analysis from four European trials comparing enprostil (35 micrograms twice daily) with cimetidine (400 mg twice daily) in the treatment of duodenal ulcer, using a double-blind, randomized design with endoscopic control. A total of 369 patients entered the trials, of whom 348 were eligible for the efficacy analyses and 362 for the safety analyses. Patients were allowed antacids as needed. The pooled cumulative healing rates at two, four, and six weeks were 40, 75, and 84 percent, respectively, for enprostil and 42, 77, and 87 percent, respectively, for cimetidine. There were no significant differences between treatments. Healing rates in both groups were reduced in smokers, in those with larger ulcers at baseline, and in those who reported a higher consumption of alcohol. Age, however, had no effect on healing rates. Digestive system complaints were reported more frequently in the enprostil group, whereas central nervous system complaints were more than twice as frequent in the cimetidine group.

Adolescent↗
PubMed1989

Effect of enprostil on glucose and lipid metabolism in type 2 diabetes.

Enprostil, a dehydro-prostaglandin E2 analogue, has been tested as treatment for peptic ulcer. Its effect on blood glucose and lipid metabolism in Type 2 diabetes was assessed in a randomized, double-blind trial. Fifteen patients on sulphonylurea therapy received, in addition, enprostil 35 micrograms or placebo thrice daily for two weeks, with a 2-week wash-out before crossover. Data from 12 patients were analysed. After a 530 Cal test breakfast at the end of active treatment, plasma glucose rose from a fasting concentration similar to that after the last placebo dose (10.5 +/- 0.8 (+/- SE) and 10.6 +/- 1.1 mmol l-1 respectively) to 1, 2 and 3 h concentrations which were 1.5 to 2.1 mmol l-1 lower than on placebo (2 h concentration 14.6 +/- 0.9 vs 16.4 +/- 1.3 mmol l-1, p less than 0.05). Serum fructosamine concentrations at the end of active treatment and placebo were 3.66 +/- 0.22 and 3.78 +/- 0.24 respectively (p = 0.051). No changes in fasting or post-prandial insulin concentrations were observed. After 2 weeks of enprostil, fasting serum triglyceride (1.76 +/- 0.18 mmol l-1) and total cholesterol (6.27 +/- 0.29 mmol l-1) concentrations were lower than after placebo (2.14 +/- 0.25 and 7.35 +/- 0.46 mmol l-1, p = 0.031 and p = 0.002, respectively), the latter effect being primarily due to reduced LDL-cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Enprostil and ranitidine in duodenal ulcer healing: double blind comparative trial.

One hundred and eighty patients with endoscopically proved duodenal ulcers were allocated at random to double blind treatment with the synthetic dehydroprostaglandin E2 enprostil 35 micrograms twice daily or ranitidine 150 mg twice daily for up to six weeks. Patients completed the study if ulcer healing and pain relief had occurred at two or four weeks. A total of 163 patients completed the trial. The duration of treatment was longer in the enprostil group (p less than 0.005) and the cumulative healing rates at two, four, and six weeks were 51%, 74%, and 85%, respectively. In the ranitidine group the corresponding figures were 65% (p less than 0.04), 89% (p less than 0.02), and 99% (p less than 0.002). More patients treated with ranitidine reported relief of pain (p less than 0.004 at weeks 5 and 6). The observed superiority of ranitidine 150 mg twice daily over enprostil 35 micrograms twice daily questions the clinical relevance of using so called "cytoprotection" as treatment for duodenal ulcer disease in the short term.

Adolescent↗
PubMed1995

Effect of enprostil and cimetidine on ethanol-induced damage to intestinal epithelial cell lines IRD 98 and IEC 17.

In addition to their inhibitory action on gastric acid secretion, prostaglandins may exert part of their protective effect on the gastrointestinal mucosa by specifically maintaining the cellular integrity of the intestinal epithelium. This in vitro study investigated the cytoprotective effect conferred on intestinal epithelial cell lines IRD 98 and IEC 17 against ethanol injury by the synthetic prostaglandin enprostil and compared effects with those of the histamine H2-receptor blocker cimetidine. Exposure to 3% ethanol (652 mM) reduced cell viability and increased the cAMP and membrane fluidity of both cell lines. Our results demonstrate that: (i) enprostil exerts a significant cytoprotective effect against damage by ethanol; (ii) cimetidine has no cytoprotective effect; (iii) IRD 98 cells are more sensitive to enprostil than IEC 17 cells.

Animals↗
PubMed1990

Ranitidine compared with the dimethylprostaglandin E2 analogue enprostil as adjunct to pancreatic enzyme replacement in adult cystic fibrosis.

In a double-blind cross-over randomized study adjunct therapy with ranitidine (2 x 150 mg) was compared with enprostil (2 x 35 micrograms) in eight adult cystic fibrosis (CF) patients receiving a fixed dose of enteric-coated microsphere capsules of pancreatin (Pancrease). The study consisted of two consecutive 14-day treatment periods. All patients kept a fixed daily fat intake during the last 5 days of each treatment period and performed 72-h faecal collections during the last 3 days of each treatment period. Gastrointestinal complaints were scored at the end of each treatment period. During treatment with ranitidine there was less faecal fat excretion (18.9% versus 25.1%; NS), less faecal weight (263 versus 303 g/day; NS), and a lower gastrointestinal complaints score (5.3 versus 3.1; P less than 0.05) compared with the treatment with enprostil. One patient dropped out during the treatment period with enprostil because of very severe diarrhoea and abdominal discomfort. We conclude from this study that adjunct therapy with ranitidine has significantly less side effects and may give a better reduction of faecal fat excretion and daily faecal weight in CF.

Adult↗
PubMedDate not supplied

Sustained enhancement of gastric HCO3 secretion in humans by enprostil.

Twelve healthy, male volunteers were treated for ten days, in double-blind conditions, with either enprostil, a PGE2 derivative, at a dose of 35 micrograms bid or with placebo. Before and after treatment fasting gastric juice was collected and basal bicarbonate secretion was measured by Feldman's method. In the enprostil group a statistically significant (p less than 0.01) increase in gastric HCO3 output was detectable 12 hours after the last dose. That finding, which is in keeping with the results of acute single-dose studies, suggests that stimulation of bicarbonate secretion by enprostil is not merely a transient phenomenon involved in the prevention of mucosal injury, but a lasting effect that may contribute to the ulcer-healing activity of the drug.

Adult↗