Park S M, Yoo B C, Lee H R, Chung H, Lee Y S
Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea.
Korean J Intern Med. 1992 Jan;7(1):1-8. doi: 10.3904/kjim.1992.7.1.1.
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.
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.
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.
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.
前列腺素E在胃黏膜中大量存在，是胃酸分泌的强效抑制剂和胃黏液分泌的刺激物。此外，前列腺素E2可抑制动物溃疡形成，其合成类似物已成功用于治疗胃溃疡和十二指肠溃疡疾病患者。为评估内源性前列腺素E2在消化性溃疡疾病发病机制中的作用，我们测定了胃溃疡和十二指肠溃疡疾病患者的黏膜前列腺素E2水平，并与非溃疡对照者进行比较。
研究人群包括44名非溃疡者、36名良性胃溃疡患者和48名十二指肠溃疡患者。从胃窦和十二指肠球部采集的每个黏膜标本均进行匀浆，与1M盐酸混合，然后离心。去除上清液后，沉淀在Amprep C18微型柱中用乙酸乙酯洗脱。然后将乙酸乙酯馏分中提取的前列腺素E2转化为其甲氧肟衍生物，并用放射免疫分析法测定前列腺素E2水平。在该过程中，任何外观明显带血的匀浆标本均从分析中剔除，以避免任何可能的污染或血液中的前列腺素E2。
在非溃疡者中，胃窦组织的平均值为258.17± 127.03 pg/mg，十二指肠球部组织为121.07± 67.46 pg/mg。胃溃疡患者相应的值分别为186.42± 70.51 pg/mg组织、79.44± 39.04 pg/mg组织，十二指肠溃疡患者为204.94± 92.03 pg/mg组织、99.66± 56.10 pg/mg组织。胃溃疡患者胃窦和十二指肠的前列腺素E2水平显著较低（p<0.005）。十二指肠溃疡患者的这些水平也显著低于非溃疡者（p<0.025和0.05）。胃溃疡患者胃窦前列腺素E2水平在溃疡愈合时升至305.21± 104.91 pg/mg组织（p<0.005），十二指肠溃疡升至271.02± 93.23 pg/mg组织（p<0.005）。十二指肠球部前列腺素E2水平在溃疡愈合阶段也升高，例如分别为128.84± 57.62（p<0.005）和112.60± 42.25 pg/mg组织。
这些结果表明，胃窦和十二指肠球部黏膜中前列腺素缺乏可能在消化性溃疡疾病发病机制中起重要作用。
