H. SUZUKI, T. MASAOKA, Y. NOMOTO, H. HOSODA, M. MORI, T. NISHIZAWA, Y. MINEGISHI, K. KANGAWA, T. HIBI
{"title":"消化性溃疡患者血浆胃饥饿素水平升高","authors":"H. SUZUKI, T. MASAOKA, Y. NOMOTO, H. HOSODA, M. MORI, T. NISHIZAWA, Y. MINEGISHI, K. KANGAWA, T. HIBI","doi":"10.1111/j.1746-6342.2006.00034.x","DOIUrl":null,"url":null,"abstract":"<div>\n \n <section>\n \n <h3> Summary</h3>\n </section>\n \n <section>\n \n <h3> Background</h3>\n \n <p>Ghrelin is a novel appetite-promoting peptide secreted primarily from the A-like cells in the gastric fundic mucosa. As gastric inflammation caused by <i>Helicobacter pylori</i> infection extends, the number of ghrelin-producing A-like cells is diminished and gastric ghrelin content decreases significantly. We previously reported that plasma levels of ghrelin, which correlated well with the serum levels of pepsinogen (PG) I and PG I/II ratio, decreased as gastric mucosal atrophy increased in non-ulcerogenic conditions and that plasma ghrelin level increased in rats with cysteamine-induced duodenal ulcer.</p>\n </section>\n \n <section>\n \n <h3> Aim</h3>\n \n <p>To investigate the plasma levels of ghrelin in patients with peptic ulcer disease.</p>\n </section>\n \n <section>\n \n <h3> Patients and Methods</h3>\n \n <p>Two hundred and eighty-six patients with epigastric symptoms, who underwent upper gastrointestinal endoscopy, were enrolled. Blood samples were collected after a 12-h fast before endoscopy. Patients were divided into four groups, namely chronic gastritis with high PG (<i>n</i> = 197), chronic gastritis with low PG (<i>n</i> = 58), duodenal ulcer (<i>n</i> = 14) and gastric ulcer (<i>n</i> = 17) and plasma concentrations of total and active ghrelin as well as serum concentrations of PG I and PG II were measured by radioimmunoassay. Six patients with duodenal ulcer and seven with gastric ulcer were also examined after ulcer healing.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>Plasma ghrelin levels were significantly higher in patients with duodenal ulcer or gastric ulcer than in those without ulcers. Elevated plasma total ghrelin levels did not significantly change after the healing of ulcers.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>Plasma ghrelin levels were significantly higher in patients with peptic ulcer than in those with gastritis without ulcer. This finding suggests a possible relationship between mucosal injury susceptibility and elevated fasting plasma ghrelin.</p>\n </section>\n </div>","PeriodicalId":50822,"journal":{"name":"Alimentary Pharmacology & Therapeutics Symposium Series","volume":"2 1","pages":"120-126"},"PeriodicalIF":0.0000,"publicationDate":"2006-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1746-6342.2006.00034.x","citationCount":"0","resultStr":"{\"title\":\"Increased levels of plasma ghrelin in peptic ulcer disease\",\"authors\":\"H. SUZUKI, T. MASAOKA, Y. NOMOTO, H. HOSODA, M. MORI, T. NISHIZAWA, Y. MINEGISHI, K. KANGAWA, T. HIBI\",\"doi\":\"10.1111/j.1746-6342.2006.00034.x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <section>\\n \\n <h3> Summary</h3>\\n </section>\\n \\n <section>\\n \\n <h3> Background</h3>\\n \\n <p>Ghrelin is a novel appetite-promoting peptide secreted primarily from the A-like cells in the gastric fundic mucosa. As gastric inflammation caused by <i>Helicobacter pylori</i> infection extends, the number of ghrelin-producing A-like cells is diminished and gastric ghrelin content decreases significantly. We previously reported that plasma levels of ghrelin, which correlated well with the serum levels of pepsinogen (PG) I and PG I/II ratio, decreased as gastric mucosal atrophy increased in non-ulcerogenic conditions and that plasma ghrelin level increased in rats with cysteamine-induced duodenal ulcer.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Aim</h3>\\n \\n <p>To investigate the plasma levels of ghrelin in patients with peptic ulcer disease.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Patients and Methods</h3>\\n \\n <p>Two hundred and eighty-six patients with epigastric symptoms, who underwent upper gastrointestinal endoscopy, were enrolled. Blood samples were collected after a 12-h fast before endoscopy. Patients were divided into four groups, namely chronic gastritis with high PG (<i>n</i> = 197), chronic gastritis with low PG (<i>n</i> = 58), duodenal ulcer (<i>n</i> = 14) and gastric ulcer (<i>n</i> = 17) and plasma concentrations of total and active ghrelin as well as serum concentrations of PG I and PG II were measured by radioimmunoassay. Six patients with duodenal ulcer and seven with gastric ulcer were also examined after ulcer healing.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>Plasma ghrelin levels were significantly higher in patients with duodenal ulcer or gastric ulcer than in those without ulcers. Elevated plasma total ghrelin levels did not significantly change after the healing of ulcers.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusions</h3>\\n \\n <p>Plasma ghrelin levels were significantly higher in patients with peptic ulcer than in those with gastritis without ulcer. 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Increased levels of plasma ghrelin in peptic ulcer disease
Summary
Background
Ghrelin is a novel appetite-promoting peptide secreted primarily from the A-like cells in the gastric fundic mucosa. As gastric inflammation caused by Helicobacter pylori infection extends, the number of ghrelin-producing A-like cells is diminished and gastric ghrelin content decreases significantly. We previously reported that plasma levels of ghrelin, which correlated well with the serum levels of pepsinogen (PG) I and PG I/II ratio, decreased as gastric mucosal atrophy increased in non-ulcerogenic conditions and that plasma ghrelin level increased in rats with cysteamine-induced duodenal ulcer.
Aim
To investigate the plasma levels of ghrelin in patients with peptic ulcer disease.
Patients and Methods
Two hundred and eighty-six patients with epigastric symptoms, who underwent upper gastrointestinal endoscopy, were enrolled. Blood samples were collected after a 12-h fast before endoscopy. Patients were divided into four groups, namely chronic gastritis with high PG (n = 197), chronic gastritis with low PG (n = 58), duodenal ulcer (n = 14) and gastric ulcer (n = 17) and plasma concentrations of total and active ghrelin as well as serum concentrations of PG I and PG II were measured by radioimmunoassay. Six patients with duodenal ulcer and seven with gastric ulcer were also examined after ulcer healing.
Results
Plasma ghrelin levels were significantly higher in patients with duodenal ulcer or gastric ulcer than in those without ulcers. Elevated plasma total ghrelin levels did not significantly change after the healing of ulcers.
Conclusions
Plasma ghrelin levels were significantly higher in patients with peptic ulcer than in those with gastritis without ulcer. This finding suggests a possible relationship between mucosal injury susceptibility and elevated fasting plasma ghrelin.