This study was aimed to investigate the association of restriction fragment length polymorphisms (RFLPs) for pepsinogen genes with peptic ulcer disease. Eighty unrelated controls, 61 patients with gastric ulcer, and 57 patients with duodenal ulcer were studied. No genetic polymorphisms for pepsinogen-A were detected by EcoRI digestion in Japanese subjects but a 100 base pairs insertion-deletion RFLP for the pepsinogen C gene was observed.The allele frequencies ofthe large (3.6 kilobase EcoRI fragment) and the small fragment (3.5 kilobase EcoRI fragment) were 80*6% and 19-4% respectively in controls, 55*4% and 44-6% in patients with gastric body ulcer, 79*4% and 20-6% in patients with gastric angular ulcer, 71*4% and 28*6% in patients with gastric antral ulcer, and 75'4% and 24.6% in patients with duodenal ulcer. The allele frequency of the smali fragment was significantly higher in patients with gastric body ulcer than in controls and in patients with gastric angular or antral ulcer. The genotypes which possessed the smali fragment were significantly more frequent in patients with gastric body ulcer (78 4%) than in controls (33 8%) and in patients with gastric angular or antral ulcer (37-5%). These results suggest that there is a significant association between the genetic polymorphism at the pepsinogen C gene locus and gastric body ulcer, and that the pepsinogen C RFLP is a useful marker of the genetic predisposition to this disorder. These results also indicate genetic heterogeneity of gastric ulcer disease, and suggest that the pepsinogen C RFLP may be a useful subclinical marker to explain the differences in genetic aetiologies of gastric body ulcer and gastric angular or antral ulcer. (Gut 1993; 34: 450-455) The basis for supposing that there are hereditary factors in the aetiology of peptic ulcer disease is provided by studies showing aggregation of peptic ulcers in the families of affected individuals to a greater extent than that found in the general population.'-3 More important information about the influence of hereditary factors in ulcer disease has been derived from studies of twins. It has been reported that the concordance rate for peptic ulcer in monozygotic twins is greater than in dizygotic twins. Since the concordance was less than 100%, the values could also be interpreted as indicating interactions between genetic predisposition and environmental factors.4 A number ofinherited characteristics, such as blood groups and HLA antigens, have been studied to determine the degree of association with peptic ulceration.5 In this connection, it is assumed that a sufficiently positive association between peptic ulceration and the allele of a defined genetic locus indicates that the genetic trait plays a part in the pathogenesis of the ulceration.
A 54-year-old man, who had no clinical symptoms, underwent a routine health checkup at our hospital. Abdominal ultrasonography disclosed a well demarcated tumor containing a solid portion occupying the dilated left hepatic duct and a cystic portion expanding into the parenchyma of the left hepatic lobe, with mild dilatation of the intrahepatic bile ducts. These findings were later confirmed by computed tomography (CT) and magnetic resonance imaging. Endoscopic retrograde cholangiography revealed a complete defect at the level of the left hepatic duct, while drip infusion cholangiographic-CT (DIC-CT) disclosed a defect of the left hepatic duct only, with the distal portions of the left intrahepatic ducts being visualized on the image. Hepatic angiography revealed light stains in the solid portion in the parenchymal phase. At left lobectomy, a multiloculated polyp-like tumor was found arising from the left hepatic duct and expanding into the parenchyma of the left hepatic lobe. Microscopically, all the lining cells in the cysts and the tumor cells in the solid portion showed the features of papillary adenocarcinoma. In this patient with extrahepatic biliary cystadenocarcinoma, DIC-CT was useful in identifying the site of origin of the tumor, and hepatic angiography was also useful in differentiating this rare malignant tumor from benign cystadenoma.
In a case of hypervascular metastatic liver tumor, the vascularity of primary focus, pancreatic carcinoma was hypovascular. Based on the imaging findings, we thought before the operation that the two lesions were double cancers. Histological examination showedthat the stromal volumeof metastatic tumoroustissue wasricher than that of the primary focus. It was suggested that the difference in the stromal volumewas related to the difference of the vascularity. Some foctors originating in stromal cells might be involved in angiogenesis. (Internal Medicine 40: 227-231, 2001)
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