Journal of Pathology and Translational Medicine

Original Articles

Relationship of Gastric Metaplasia of the Duodenum with Age, Duodenal Ulcer and Helicobacter pylori Infection.: Dae Hyun Song, Dong Chul Kim, Jong Sil Lee, Jeong Hee Lee, Hyun Jin Kim, Hee Shang Youn, Gyung Hyuck Ko; Korean J Pathol. 2007;41(4):217-223.

Abstract PDF: BACKGROUND
Gastric metaplasia of the duodenum is thought to be associated with the pathogenesis of duodenal ulcer. We investigated the pathological features of gastric metaplasia and their relation to age, gender, duodenal ulcer and H. pylori infection.
METHODS
We reviewed the duodenal endoscopic findings of 535 patients (age range: 0 to 87) and the microscopic slides of the duodenal biopsy specimens.
RESULTS
Gastric metaplasia was first noted at the age of 4 and the prevalence increased thereafter until the patients' mean age reached about 30. The prevalence of gastric metaplasia was 53.7% after 30 years of age. As the metaplasia became severer, it became more polypoid in appearance and it more often contained parietal cells. Gastric metaplasia was more frequently observed or severe in duodenal ulcer patients, in males and in the first portion of the duodenum than in patients without duodenal ulcer, in females and in the second portion, respectively. There was a lack of correlation between gastric metaplasia and H. pylori infection.
CONCLUSIONS
The prevalence and/or severity of gastric metaplasia of the duodenum increases with age, and it is thought that most duodenal ulcers develop in the areas of gastric metaplasia.

An Experimental Study of Pathogenesis of Duodenal Ulceration Produced by Mepirizole.: Myung Jae Kang, Jae Ryong Jung, Hye Soo Lee, Sang Ho Kim; Korean J Pathol. 1988;22(4):383-392.

Abstract PDF: To investigate the pathogenesis of the duodenal ulceration produced by mepirizole (1-(4-methoxy-6-methyl-2-pyrimidinyl)-3-methyl-5-methoxypyrazole) in rat, the effects of various concentraion and sorts of antiulcer drugs and truncal vagotomy on the mepirizole (200 mg/kg of body weight) induced duodenal ulcers were observed morphologically, and after mepirizole administration (200 mg/kg), amount and acidity of gastric jucie were measured sequently. The results were as follows: 1) In the control group of fasting for 24 hours after mepirizole administration only, duodenal ulcers were developed in all animals with 21.5+/-5.8 mm2 of ulcer index, perforation rate was 15%, and mortality rate was 0%. But lesions of the stomach were hemorrhagic and erosive with erosion index of 3.8+/-1.6 mm2. 2) The antiulcer drugs were significantly inhibited duodenal ulceration and gastric erosion produced by mepirizole although the inhibition effects were different. 3) After truncal vagotomy, duodenal ulcer and gastric erosion induced by mepirizole were also significantly inhibited. 4) On the gastric analysis, decrease of amount, increase of acidity, and decrease of concentration of gastric juice were observed after administration of mepirizole compared with nontreated normal group. Above findings suggest that the pathogenesis of the duodenal ulceration by mepirizole is the action of gastric acid on the duodenal mucosa with breakdown of defence mechanisms of the duodenum.

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