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Distribution of prostaglandin E2 in gastric and duodenal mucosa: possible role in the pathogenesis of peptic ulcer.

Park SM, Yoo BC, Lee HR, Chung H, Lee YS - Korean J. Intern. Med. (1992)

Bottom Line: In addition, prostaglandin E2 inhibits ulcer formation in animals, and the synthetic analogues of prostaglandin E have successfully been used in the treatment of patients with gastric and duodenal ulcer disease.To evaluate the role of endogenous prostaglandin E2 in the pathogenesis of the peptic ulcer disease, we measured mucosal prostaglandin E2 levels in patients with gastric and duodenal ulcer disease and compared with that of non-ulcer control persons.These results suggest that prostaglandin deficiency in the antral and duodenal bulb mucosa may have an important role in the pathogenesis of peptic ulcer disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea.

ABSTRACT

Background: Prostaglandin E which is present abundantly in the gastric mucosa is a powerful inhibitor of gastric acid secretion and a stimulus to gastric mucus production. In addition, prostaglandin E2 inhibits ulcer formation in animals, and the synthetic analogues of prostaglandin E have successfully been used in the treatment of patients with gastric and duodenal ulcer disease. To evaluate the role of endogenous prostaglandin E2 in the pathogenesis of the peptic ulcer disease, we measured mucosal prostaglandin E2 levels in patients with gastric and duodenal ulcer disease and compared with that of non-ulcer control persons.

Methods: The study population was made up of 44 non-ulcer persons, 36 patients with a benign gastric ulcer, and 48 with a duodenal ulcer. Every mucosal specimen, taken from the antrum and from the duodenal bulb, were homogenized, mixed with 1 M HCl, and centrifuged. After removal of the supernatant, precipitate was eluted with ethyl acetate in the Amprep C18 minicolumn. Then the extracted prostaglandin E2 in the ethyl acetate fractions was converted into its methyl oximate derivatives, and the prostaglandin E2 level was measured by radioimmunoassay. During the procedure any homogenized specimen which was looking grossly bloody was removed from the assay in order to avoid any possible contamination or prostaglandin E2 in blood.

Results: In non-ulcer persons, the mean values was 258.17 +/- 127.03 pg/mg. tissue in antrum and 121.07 +/- 67.46 pg/mg. tissue in duodenal bulb. The corresponding values were 186.42 +/- 70.51 pg/mg. tissue, 79.44 +/- 39.04 pg/mg. tissue in gastric ulcer patients and 204. 94 92.03 pg/mg. tissue, 99.66 +/- 56.10 pg/mgl. tissue in duodenal ulcer patients respectively. Gastric ulcer patients have the significantly lower level of the antral and duodenal prostaglandin E2 (p < 0.005). Those levels of duodenal ulcer patients were also significantly lower than those of non-ulcer persons (p < 0.025 & 0.05). Antral prostaglandin E2 level increased to 305.21 +/- 104.91 pg/mg. tissue in the gastric ulcer patients (p < 0.005) and to 271.02 +/- 93. 23 pg/mg. tissue in the duodenal ulcer (p < 0.005) when the ulcer crater was healed. The duodenal bulb prostaglandin E2 level was also increased in the healed stage of ulcer, e. g., 128.84 +/- 57.62 (p < 0.005) and 112.60 +/- 42.25 pg/mg. tissue, respectively.

Conclusion: These results suggest that prostaglandin deficiency in the antral and duodenal bulb mucosa may have an important role in the pathogenesis of peptic ulcer disease.

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Mucosal prostaglandin E2 levels in patients with the gastric ulcer before and after their ulcers were healed. Both the antral and duodenal PG E2 are significantly increased when ulcers are healed. (antrum; p<0.005 duodenal bulb; p<0.005)
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f2-kjim-7-1-1-1: Mucosal prostaglandin E2 levels in patients with the gastric ulcer before and after their ulcers were healed. Both the antral and duodenal PG E2 are significantly increased when ulcers are healed. (antrum; p<0.005 duodenal bulb; p<0.005)

Mentions: In the 44 non-ulcer persons studied, the anrum contained 258.17±127.03 (97.14–548.83) pg/mg. tissue and the duodenal bulb 121.07±67.46 (45.00–357.14). The antrum contained significantly higher concentration of PGE2 than the duodenal bulb (p<0.005) (Table 2 and Fig. 1). In the 37 patients with benign gastric ulcer the antrum contained 186.42±70.51 (55.71–396.55) pg/mg. tissue and the duodenal bulb 79.44±39.04 (32.64–202.50). These were also significantly different from each other (p<0.005). In gastric ulcer patients PGE2 concentrations of both the antral and the duodenal bulb were significantly lower than the respective levels in the non-ulcer persons (p<0.005) (Table 2 and Fig. 1). In the 48 patients with active duodenal ulcer the PGE2 concentration were 204.94±92.03 (39.68–400.00) pg/mg. tissue in the antrum and 99.66±56.10 (36.36–291.43). in the duodenal bulb. These were also significantly different from those of non-ulcer persons (p<0.025 & p<0.05) (Table 2 and Fig. 1). All patiets with either the gastric or the duodenal ulcer were completely healed after 4 to 7-week treatment with the H2-receptor blocking drug (Ranitidine 300 mg/day, at bed time) in combining with or without the liquid antacid (Mylanta 40 ml to 70 ml a day). There was no significant difference between the location of ulcer and the healing rate. Table 3, figure 2 and 3 showed the antral and the duodenal bulb concentration of PGE2 before and after healing of the ulcer crater. As a group, tissue levels of PGE2, except for those of duodenal bulb PGE2 in the duodenal ulcer patients, were significantly increased when the ulcer was healed in both the gastric and the duodenal ulcer patients. Antral PGE2 levels in the active and healed stage of ulcer were 186.42±70.51 vs 305.21±104.91 (p<0.005) in the gastric ulcer patients and 204.94±92.03 vs 271.02±93.23 pg/mg. tissue (p<0.005) in the duodenal ulcer, respectively. The corresponding levels of the duodenal bulb were 79.44±39.04 vs 128.84±57.62 (p<0.005) and 99.66±56.10 vs 112.60±42.25 pg/mg. tissue (p<0.25). When the tissue PGE2 level were measured in same patients before and after the ulcer healing, both the antral and the duodenal PGE2 levels still showed significant difference between the active and the healed stage of ulcer (p<0.025 for GU and p<0.005 for DU) (Table 4 and Fig. 4). Although the difference in the bulb PGE2 in duodenal ulcer patients between different stages of ulcer seemed to be contradictory in each investigation, this might be resulted from the disparity of the study population in each group.


Distribution of prostaglandin E2 in gastric and duodenal mucosa: possible role in the pathogenesis of peptic ulcer.

Park SM, Yoo BC, Lee HR, Chung H, Lee YS - Korean J. Intern. Med. (1992)

Mucosal prostaglandin E2 levels in patients with the gastric ulcer before and after their ulcers were healed. Both the antral and duodenal PG E2 are significantly increased when ulcers are healed. (antrum; p<0.005 duodenal bulb; p<0.005)
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4532093&req=5

f2-kjim-7-1-1-1: Mucosal prostaglandin E2 levels in patients with the gastric ulcer before and after their ulcers were healed. Both the antral and duodenal PG E2 are significantly increased when ulcers are healed. (antrum; p<0.005 duodenal bulb; p<0.005)
Mentions: In the 44 non-ulcer persons studied, the anrum contained 258.17±127.03 (97.14–548.83) pg/mg. tissue and the duodenal bulb 121.07±67.46 (45.00–357.14). The antrum contained significantly higher concentration of PGE2 than the duodenal bulb (p<0.005) (Table 2 and Fig. 1). In the 37 patients with benign gastric ulcer the antrum contained 186.42±70.51 (55.71–396.55) pg/mg. tissue and the duodenal bulb 79.44±39.04 (32.64–202.50). These were also significantly different from each other (p<0.005). In gastric ulcer patients PGE2 concentrations of both the antral and the duodenal bulb were significantly lower than the respective levels in the non-ulcer persons (p<0.005) (Table 2 and Fig. 1). In the 48 patients with active duodenal ulcer the PGE2 concentration were 204.94±92.03 (39.68–400.00) pg/mg. tissue in the antrum and 99.66±56.10 (36.36–291.43). in the duodenal bulb. These were also significantly different from those of non-ulcer persons (p<0.025 & p<0.05) (Table 2 and Fig. 1). All patiets with either the gastric or the duodenal ulcer were completely healed after 4 to 7-week treatment with the H2-receptor blocking drug (Ranitidine 300 mg/day, at bed time) in combining with or without the liquid antacid (Mylanta 40 ml to 70 ml a day). There was no significant difference between the location of ulcer and the healing rate. Table 3, figure 2 and 3 showed the antral and the duodenal bulb concentration of PGE2 before and after healing of the ulcer crater. As a group, tissue levels of PGE2, except for those of duodenal bulb PGE2 in the duodenal ulcer patients, were significantly increased when the ulcer was healed in both the gastric and the duodenal ulcer patients. Antral PGE2 levels in the active and healed stage of ulcer were 186.42±70.51 vs 305.21±104.91 (p<0.005) in the gastric ulcer patients and 204.94±92.03 vs 271.02±93.23 pg/mg. tissue (p<0.005) in the duodenal ulcer, respectively. The corresponding levels of the duodenal bulb were 79.44±39.04 vs 128.84±57.62 (p<0.005) and 99.66±56.10 vs 112.60±42.25 pg/mg. tissue (p<0.25). When the tissue PGE2 level were measured in same patients before and after the ulcer healing, both the antral and the duodenal PGE2 levels still showed significant difference between the active and the healed stage of ulcer (p<0.025 for GU and p<0.005 for DU) (Table 4 and Fig. 4). Although the difference in the bulb PGE2 in duodenal ulcer patients between different stages of ulcer seemed to be contradictory in each investigation, this might be resulted from the disparity of the study population in each group.

Bottom Line: In addition, prostaglandin E2 inhibits ulcer formation in animals, and the synthetic analogues of prostaglandin E have successfully been used in the treatment of patients with gastric and duodenal ulcer disease.To evaluate the role of endogenous prostaglandin E2 in the pathogenesis of the peptic ulcer disease, we measured mucosal prostaglandin E2 levels in patients with gastric and duodenal ulcer disease and compared with that of non-ulcer control persons.These results suggest that prostaglandin deficiency in the antral and duodenal bulb mucosa may have an important role in the pathogenesis of peptic ulcer disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea.

ABSTRACT

Background: Prostaglandin E which is present abundantly in the gastric mucosa is a powerful inhibitor of gastric acid secretion and a stimulus to gastric mucus production. In addition, prostaglandin E2 inhibits ulcer formation in animals, and the synthetic analogues of prostaglandin E have successfully been used in the treatment of patients with gastric and duodenal ulcer disease. To evaluate the role of endogenous prostaglandin E2 in the pathogenesis of the peptic ulcer disease, we measured mucosal prostaglandin E2 levels in patients with gastric and duodenal ulcer disease and compared with that of non-ulcer control persons.

Methods: The study population was made up of 44 non-ulcer persons, 36 patients with a benign gastric ulcer, and 48 with a duodenal ulcer. Every mucosal specimen, taken from the antrum and from the duodenal bulb, were homogenized, mixed with 1 M HCl, and centrifuged. After removal of the supernatant, precipitate was eluted with ethyl acetate in the Amprep C18 minicolumn. Then the extracted prostaglandin E2 in the ethyl acetate fractions was converted into its methyl oximate derivatives, and the prostaglandin E2 level was measured by radioimmunoassay. During the procedure any homogenized specimen which was looking grossly bloody was removed from the assay in order to avoid any possible contamination or prostaglandin E2 in blood.

Results: In non-ulcer persons, the mean values was 258.17 +/- 127.03 pg/mg. tissue in antrum and 121.07 +/- 67.46 pg/mg. tissue in duodenal bulb. The corresponding values were 186.42 +/- 70.51 pg/mg. tissue, 79.44 +/- 39.04 pg/mg. tissue in gastric ulcer patients and 204. 94 92.03 pg/mg. tissue, 99.66 +/- 56.10 pg/mgl. tissue in duodenal ulcer patients respectively. Gastric ulcer patients have the significantly lower level of the antral and duodenal prostaglandin E2 (p < 0.005). Those levels of duodenal ulcer patients were also significantly lower than those of non-ulcer persons (p < 0.025 & 0.05). Antral prostaglandin E2 level increased to 305.21 +/- 104.91 pg/mg. tissue in the gastric ulcer patients (p < 0.005) and to 271.02 +/- 93. 23 pg/mg. tissue in the duodenal ulcer (p < 0.005) when the ulcer crater was healed. The duodenal bulb prostaglandin E2 level was also increased in the healed stage of ulcer, e. g., 128.84 +/- 57.62 (p < 0.005) and 112.60 +/- 42.25 pg/mg. tissue, respectively.

Conclusion: These results suggest that prostaglandin deficiency in the antral and duodenal bulb mucosa may have an important role in the pathogenesis of peptic ulcer disease.

Show MeSH
Related in: MedlinePlus