與幽門螺旋桿菌有關之十二指腸潰瘍，潰瘍治療前後，Cu/Zn-Superoxide dismutase(SOD) 及Prostaglandin E2(PGE2) 含量與胃炎嚴重度之關係 本實驗是研究與幽門螺旋桿菌有關之十二指腸潰瘍，潰瘍治療前後，Cu/Zn-Superoxide dismutase(SOD)

Presentation on theme: "與幽門螺旋桿菌有關之十二指腸潰瘍，潰瘍治療前後，Cu/Zn-Superoxide dismutase(SOD) 及Prostaglandin E2(PGE2) 含量與胃炎嚴重度之關係 本實驗是研究與幽門螺旋桿菌有關之十二指腸潰瘍，潰瘍治療前後，Cu/Zn-Superoxide dismutase(SOD)"— Presentation transcript:

1 與幽門螺旋桿菌有關之十二指腸潰瘍，潰瘍治療前後，Cu/Zn-Superoxide dismutase(SOD) 及Prostaglandin E2(PGE2) 含量與胃炎嚴重度之關係
本實驗是研究與幽門螺旋桿菌有關之十二指腸潰瘍，潰瘍治療前後，Cu/Zn-Superoxide dismutase(SOD) 及 Prostaglandin E2(PGE2) 含量與胃炎嚴重度之關係◦ 我們選擇40位急性十二指腸潰瘍(A2 stage)合併胃炎之幽門螺旋桿菌感染患者，其中男、女性各20位，在平均年齡及男女性別上，均無統計學上有意義之差異◦ 在這40位患者中，先施予三合一療法(Cimetidine, Metronidazole, Amoxicillin) 二週之治療，然後再給予Cimetidine四週◦ 治療前後，分別從距幽門環(pyloric ring) 5公分內之胃前庭黏膜較紅處，各取四片胃黏膜組織切片◦ 幽門螺旋桿菌存在與否，以快速尿素試驗(如CLO test)、病理組織切片(H & E stain)及13C尿素呼氣試驗(UBT) 來證實◦ 胃炎的嚴重程度是依照The modified Sydney System，檢查胃黏膜組織的五項型態，包括Inflammation、Activity、Atrophy、Intestinal metaplasia及H. Pylori，每項再依程度不同，分成Normal, Mild, Moderate, Severe四級，依序給予0,1,2,3 分，最後再統計總分◦ 十二指腸潰瘍患者胃黏膜中Cu/Zn—Superoxide dismutase (SOD)及 Prostaglandin E2(PGE2)，在治療前後皆給予ELISA法測定◦ 結果顯示，潰瘍經三合一療法治療後，胃黏膜組織中Cu/Zn-Superoxide dismutase(SOD) 及 Prostaglandin E2(PGE2)比潰瘍治療前有較高之含量， 在統計學上呈有意義之差異(P<0.05)◦ 在潰瘍治療後，The Sydney System有較低的平均分數，在統計學上呈有意義之差異(P<0.05) ◦ 潰瘍治療後，比較幽門螺旋桿菌根除組及未根除組，前者胃黏膜組織中Cu/Zn-Superoxide dismutase(SOD) 及 Prostaglandin E2(PGE2) 均有較高之含量，The Sydney System有較低的平均分數，在統計學上呈有意義之差異(P<0.05)◦ 我們的結論是:與幽門螺旋桿菌有關之十二指腸潰瘍及胃炎，當十二指腸潰瘍及胃炎較嚴重時，胃黏膜組織中Cu/Zn-SOD及PGE2含量較少，潰瘍經治療後，十二指腸潰瘍及胃炎較輕微時，胃黏膜組織中Cu/Zn-SOD及PGE2含量較多◦ 幽門螺旋桿菌根除與否，會影響Cu/Zn-SOD及PGE2的含量◦

2 A study was conducted by our institute to clarify the hypothesis that the severity of gastritis was associated with the level of Cu/Zn-superoxide dismutase (SOD) and prostaglandin E2 (PGE2) in H. Pylori related duodenal ulcer. Total of 40 patients with active duodenal ulcer (A2 ulcer) and gastritis with H. Pylori infection were involved in the study. Among them were 20 male and 20 female. There was no significant difference in average age and gender. The patients received triple therapy (medication with Cimetidine 400 mg bid, Metronidazole 250 mg qid and Amoxicillin 500 mg qid) for two weeks, followed by Cimetidine 400 mg bid for four weeks. Before and after medical treatment, four biopsy specimens were taken from the antral mucosa, within 5 cm from pyloric ring. For evaluation of H. Pylori infection rate, that CLO test, histological examination (with H & E stain) and 13C -UBT test were used. The severity of gastritis was assessed by the modified Sydney System. The morphology of gastric mucosa was classified into five groups, inflammation、activity、atrophy、intestinal metaplasia and H. Pylori. According to the severity, each group was divided into four grades; normal, mild, moderate and severe. The score 0,1,2,3 was given to each grade respectively. We then calculated the summation of total scores. For detection of Cu/Zn-superoxide dismutase (SOD) and prostaglandin E2 (PGE2) levels, ELISA was used. The results showed that after treatment of acute duodenal ulcer, there was a significant higher content of Cu/Zn-superoxide dismutase (SOD) and prostaglandin E2 (PGE2) in gastric mucosa of the patients (P<0.05). Correspondingly, there was also a significant lower score by the Sydney system (P<0.05). After eradication of H. Pylori, there was a significant higher level of Cu/Zn-superoxide dismutase (SOD), prostaglandin E2 (PGE2), and a lower score by the Sydney System (P<0.05). In conclusion, in H. Pylori related duodenal ulcer, there are lower levels of Cu/Zn-superoxide dismutase (SOD) and prostaglandin E2 (PGE2) in gastric mucosa during severe duodenal ulcer and gastritis. After H. Pylori eradication, the higher level of Cu/Zn-superoxide dismutase (SOD) and prostaglandin E2 (PGE2) in gastric mucosa corresponds to the resolution of duodenal ulcer and gastritis.