Background : Various types of classification of gastritis have been proposed, but no plausible classification has been available until now. The Research Society for Gastritis performed a pilot study to establish an endoscopic classification, taking into consideration the following: (i) ease of use; (ii) permitting everyone the common image; and (iii) presence of histopathological evidence. Methods : One hundred and fifty-five patients were enrolled and underwent gastroscopy. Eight basic endoscopic and histological types of gastritis (superficial, hemorrhagic, erosive, verrucous, atrophic, metaplastic, hyperplastic and special types) were defined. Gastritis was endoscopically diagnosed according to the definition of the endoscopic types of gastritis. Four or more biopsy specimens were obtained from the lesser and the greater curvatures of the antrum and the corpus of each patient, and the histological findings of gastritis and Helicobacter pylori infection were assessed. The histological diagnosis of gastritis was made according to the definition of histology types of gastritis. The endoscopic and the histological diagnoses were then compared in a blinded fashion. Results : Endoscopic diagnosis was 62% as sensitive as histological diagnosis for erosive gastritis, 67% for verrucous gastritis and 84% for atrophic gastritis in the antrum. In superficial gastritis, sensitivity was approximately 25% in the corpus, but only 8% in the antrum. Metaplastic and hyperplastic gastritis were correctly diagnosed only in severe cases. Conclusion : Five basic types of gastritis (superficial, erosive, verrucous, atrophic and special types) should be employed for the new endoscopic gastritis classification. Metaplastic and hyperplastic gastritis are considered to be subtypes of atrophic gastritis and they should be excluded from the basic endoscopic classification. A new definition of gastritis in the antrum accompanied by redness still remains to be investigated.
Celiac axis stenosis is frequently associated with pancreaticoduodenal artery aneurysms. Although the cause of stenosis was not clear in most of the reported cases, compression of the median arcuate ligament of the diaphragm was found to be responsible for the stenosis in 7 of 42 reported cases of this type of aneurysm. We report a case of aneurysm caused by compression of the median arcuate ligament of the diaphragm and celiac plexus. An asymptomatic 43-year-old Japanese man was admitted with a low echoic lesion in the uncus of pancreas. Computed tomographic scan and angiogram revealed stenosis of the celiac axis and two aneurysms in the inferior posterior pancreaticoduodenal artery. The celiac plexus and median arcuate ligament were divided surgically and normal flow was reestablished in the celiac axis. One of the aneurysms was resected and the afferent artery of the other aneurysm was ligated. In the setting of pancreaticoduodenal artery aneurysm associated with celiac axis stenosis, management of stenosis should be considered in addition to local treatment of the aneurysm. In this context, division of median arcuate ligament and celiac plexus or aorto-celiac bypass may normalize the flows in the pancreaticoduodenal arcade and could be effective in preventing aneurysm reformation.
Aim : To evaluate the efficacy of polaprezinc, a mucosal protective agent, in combination with a 7‐day triple therapy containing lansoprazole, amoxycillin and clarithromycin, as a treatment for Helicobacter pylori. Methods : Sixty‐six consecutive patients suffering from dyspeptic symptoms with H. pylori infection were randomly allocated to one of two regimens: one group (LAC; n = 31) received lansoprazole 30 mg b.d., amoxycillin 500 mg b.d. and clarithromycin 400 mg b.d. for 7 days. The other group (LACP; n = 35) received the LAC regimen plus polaprezinc 150 mg b.d. for 7 days. H. pylori status was evaluated by rapid urease test, histology and culture at entry and 4 weeks after treatment. Results : Five patients did not complete the treatment: no follow‐up endoscopy was performed on two patients in the LAC group; one patient in the LAC group and two in the LACP group had their treatment stopped due to severe diarrhoea. By per protocol analysis, H. pylori eradication was achieved in 24 of the 28 evaluable patients (86%; 95% CI: 72–100%) after LAC therapy, and in 33 of the 33 evaluable patients (100%) after LACP therapy (P < 0.05). On intention‐to‐treat analysis, the rates of eradication were 24 of 31 patients (77%; 95% CI: 62–93%) in the LAC group, and 33 of 35 patients (94%; 95% CI: 86–100%) in the LACP group (P < 0.05). Conclusion : A 7‐day triple therapy with lansoprazole, amoxycillin and clarithromycin is effective in H. pylori eradication, but this regimen is significantly improved by the addition of polaprezinc.
We report herein the case of a 44-year-old man in whom an asymptomatic dissecting aneurysm was found in the proximal part of the superior mesenteric artery (SMA) during a preoperative evaluation for colon cancer. The patient was managed conservatively with blood pressure control during the perioperative period of the colon resection as the false lumen of the dissecting aneurysm was revealed to be completely occluded by thrombus. The thrombus in the false lumen continued to be absorbed until 1 month after surgery. The patient is currently well 4 years after his operation without any evidence of recurrence of the aneurysm.
To investigate whether submucosally applied endothelin-1 (ET-1) can induce gastric ulcer, ET-1 (62.5, 125, 250, and 500 pmol/kg) was injected in the submucosal layer of the rat gastric body. Twenty-four hours later, gastric ulcer (ulcer area: 10.31 +/- 5.13 mm2, mean +/- SE, at 500 pmol/kg, n = 8) was induced. The mucosal damage induced by the two highest doses was present even at 2 wk after their injection. Measurement of the mucosal blood flow at the injected area with three different methods (laser-Doppler flowmetry, hydrogen gas clearance, and reflectance spectrophotometry) revealed that injected ET-1 produced an extremely long-lasting vasoconstriction. Pretreatment with nicardipine, a Ca(2+)-channel blocker (1 mg/kg iv), significantly attenuated the ET-1-induced mucosal damage as well as the decrease in mucosal blood flow. Pretreatment with omeprazole (5-40 mumol/kg) also, significantly attenuated the ET-1-induced mucosal damage. Combined pretreatment with omeprazole (40 mumol/kg) and nicardipine almost abolished the ET-1-induced damage. The present study shows that a novel model for experimental ulcers can be induced by submucosal injection of ET-1.
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