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Gastrogastric fistula is an extremely rare complication of benign gastric ulcer. We report a case of gastrogastric fistula in a 67-year-old male who presented with symptoms of dyspnea on exertion, pretibial pitting edema, and dyspepsia. He suffered from a peptic ulcer 9 years ago and from a gastric outlet obstruction 5 years ago. A gastrogastric fistula was observed by endoscopy, and the biopsy forceps were passed through the fistulous tract. The patient was treated with proton pump inhibitors, and H. pylori was eradicated. Gastrogastric fistula, unlike other types of gastric fistulas, can be cured using non-surgical therapy as long as complications such as peritonitis, gastric outlet obstruction, and bleeding do not occur. (Korean J Gastrointest Endosc 2006;33:364 367)
Background/Aims : It has been reported that the difference in the hepatitis C virus (HCV) genotype due to genetic heterogeneity of HCV influence the clinical features, prognosis of HCV associated liver disease and response to interferon therapy. Prevalence of different genotypes of HCV may also vary between geographic areas. The aim of this study was to examine the relationship between the response to interferon alpha (IFN-α) therapy and HCV genotypes in patients with chronic HCV infection in Taegu and its environs. Methods : One hundred seventy six patients known to be HCV antibody and HCV-RNA positive were evaluated for HCV genotypes by restriction fragment length polymorphism. Among patients who had elevated ALT levels, 67 patients have been investigated for the role of the HCV genotype on disease outcome and the response of IFN-α therapy. Results : Genotype 1b were found in 59.0% of patients (103/176), genotype 2a in 37.5% (66/176). The mode of transmission of HCV infection was guessed as transfusion inenotype 1b, but as parenteral infection in genotype 2a. According to their response to IFN-α therapy, 73 patients were divided into three groups, complete response, 18 (60%) of 30 patients with genotype 2a and 21 (48.8%) of 43 patients with genotype 1b: partial response, 5 (16.7%) of 30 patients with genotype 2a and 7 (16.2%) of 43 patients with genotype 1b: no response, 7 (23.3%) of 30 patients with genotype 2a and 15 (34.9%) of 43 patients with genotype 1b. Good response to IFN-α therapy was observed among patients group showing normal platelet count in patients with genotype 1b and normal GGT in patients with genotype 2a. Conclusions: The most frequently identified genotype was genotype 1b in Taegu and its environs, followed by genotype 2a. The HCV genotype was not a reliable predictor of response to IFN-α therapy. When a standardized regimen of IFN-α was administered, pretreatment serum platelet counts and GGT level seem to be useful predictor of IFN-α therapy in HCV infection. Further investigationsrequired in order to establish a correlation between viral factors and therapeutic responses. (Korean J Hepatol 1999;5:22-32)
Background: Cholestatic hepatitis is failure of bile to reach the duodenum with hepatocellular damage and no demonstrable obstruction of the major bile ducts. The prognosis is usually good with recovery in less than 4 weeks after withdrawal of the offending drug. However, a prolonged course lasting over 3 months is possible and, in rare cases, progression to ductopenia with development of a vanishing bile duct syndrome occurs. A differential diagnosis with other causes of Chronic liver disease is needed. Materials and Methods: From January 1991 through Jaunary 2000, 14 patients diagnosed as cholestatic hepatitis by liver biopsy were inclouded. The possible causative drug, clinical features, laboatory findings, and progression of cholestatic hepatitis were evaluated. The semiquantitative study of liver lesions was performed by two independent observers. Results: Causes of cholestatic hepatitis are 5 cases of oriental medicine, 3 cases of anti-tuberculosis medication, 1 case of ticlopidine and antibiotics and 4 cases of unknown causes. The clinical features of cholestatic hepatitis were jaundice, itching, urine color change, and general weakness. During 6 to 30 months, LFT of 5 patients showed prolonged elevation. Elevated total cholesterol ≥250 mg/dL in 6 patients, pheripheral blood eosinophilia in 5 patients, auto-antibody positive in 6 patients were observed respectively. The biopsies showed intralobular bilirubinostasis with a mixed portal inflammatory infiltration. Conclusion: In cholestatic hepatitis. durations of abnormal LFT are variable regardless of causative drugs. If cholestatic hepatitis progresses toward chronic course, viral hepatitis, primary biliary cirrhosis, and autoimmune hepatitis should be differentially diagnosed and sequential liver biopsies are needed.