Background and aims-The genetic trait plays a part in the pathogenesis of peptic ulcer disease. To identify a DNA marker for peptic ulcer disease, the association between the restriction fragment length polymorphism (RFLP) of the pepsinogen C (PGC) gene and peptic ulcer disease was investigated. Patients and methods-One hundred and seventy seven unrelated controls, 75 patients with gastric ulcer, and 70 with duodenal ulcer were studied. PGC-RFLP was analysed by polymerase chain reaction (PCR), and the association between PGC-RFLP and peptic ulcer disease was examined. The relation between the genetic association of PGC polymorphism with peptic ulcer and Helicobacter pylori infection was also examined. Results-Four alleles, 480 (allele 1), 450 (allele 2), 400 (allele 3), and 310 bp (allele 4), were detected by PCR. The frequency of allele 4 was significantly higher in patients with gastric body ulcer than in controls ( 2 =9.92, p<0.005). Genotypes containing allele 4 were significantly more frequent in patients with gastric body ulcer than in controls and patients with gastric angular or antral ulcer. The relative risk of gastric body ulcer associated with the presence of allele 4, compared with its absence, was 4.63 and was statistically significant ( 2 =14.84, p<0.005). There were no significant diVerences in the allelic frequencies between H pylori positive and H pylori negative groups in controls, patients with gastric body ulcer, or patients with gastric angular or antral ulcer. Both in H pylori negative and H pylori positive cases, there was an increased frequency of allele 4 in patients with gastric body ulcer compared with controls. Conclusions-These results suggest that there is a significant association between this genetic polymorphism at the PGC gene locus and gastric body ulcer. There are diVerences in the genetic aetiology between gastric body ulcer and gastric angular or antral ulcer. PGC-RFLP may be used as a genetic marker for a genetic predisposition to gastric body ulcer; this genetic predisposition is not associated with H pylori infection. (Gut 1997; 41: 469-474)
We report a patient with transient periduodenal panniculitis due to spontaneous rupture of a pancreatic pseudocyst into the duodenum. He developed sudden onset of severe epigastric and back pain with jaundice, mimicking the symptoms of acute pancreatitis. However, the serum and urinary amylase levels did not increase. CT scans showed disappearance of his pseudocyst and periduodenal panniculitis without any evidence of acute pancreatitis. The CT findings of periduodenal panniculitis and his symptoms both improved within 3 weeks. A duodenal fistula leading to the remnant pseudocyst and narrowing of the periduodenal portion of the common bile duct were demonstrated by endoscopic retrograde cholangiopancreatography.
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