Endoscopic "clip and cut" diverticulotomy for a giant midesophageal diverticulum.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Jae Seon Kim.
Explore the source record for details and available documents.
BACKGROUND: An ectopic opening of the common bile duct in the duodenal bulb is extremely rare, and the clinical significance of this anomaly has not been clarified. This study analyzed the clinical implications and cholangiographic findings of this anomaly. METHODS: A total of 18 patients (15 men, 3 women; median age, 51 years) with an ectopic opening of the common bile duct in the duodenal bulb were studied. Medical records, endoscopic findings, and cholangiographic and other radiographic findings were reviewed. RESULTS: All 18 patients had biliary pain; 7 had fever and chills. Fifteen (83%) had diffuse dilatation of the extrahepatic bile ducts with or without intrahepatic bile duct dilation. Associated bile duct stones were found in 10 (56%) patients. The papilla in the bulb had an orifice stained with bile at endoscopy, which was associated with duodenal ulcer disease found in 13 (72%) patients. The distal end of the common bile duct was tapered and narrowed and had a hook shape in all patients. CONCLUSION: An ectopic opening of the common bile duct in the duodenal bulb may be associated with clinical entities such as recurrent or intractable duodenal ulcer, choledocholithiasis, or acute cholangitis. Although these openings are rare, knowledge of the endoscopic and radiographic findings of an ectopic opening of the common bile duct in the duodenal bulb may help to clarify the cause of chronic recurrent duodenal ulcer disease in some patients and prevent damage to the bile duct during surgery.
We report a case of pathologically proven simultaneous duodenal and colonic metastases about four years after nephrectomy for mixed clear and granular cell type renal cell carcinoma (RCC). A 76-year-old female patient who had undergone a left radical nephrectomy 4 years previously for RCC presented with a 1-month history of dyspepsia and pain in the right upper abdomen. An abdominopelvic CT scan showed circumferential wall thickening with high enhancement at the second portion of the duodenum and additional enhancement of an irregular protruding mass into the lumen of the ascending colon. A gastroscopy showed a large and ulcerative protruding mass nearly obstructing the second portion of the duodenum. A colonoscopy revealed a polypoid, nodular and purplish mass in the ascending colon. Microscopy of the biopsy specimen showed the features identical to those of the RCC which was resected 4 years earlier in this patient. We believe this to be the first case illustrating a metastatic renal cell carcinoma as simultaneous duodenal and colon masses.
BACKGROUND: It has been reported that there are four zones of distinct venous patterns around the gastroesophageal junction (GEJ); i.e. truncal, perforating, palisade (PZ) and gastric zones. Using the distal end of PZ as a marker for GEJ, this study was done to assess the length and patterns of PZ in Koreans, and to assess the prevalence of endoscopic Barrett's esophagus (E-BE) and hiatal hernia (E-HH). METHODS: 847 consecutive patients undergoing diagnostic endoscopy were included. During endoscopy, PZ, squamocolumnar junction (SCJ) and pinchcock action (PCA) were identified. Patterns were classified according to the relationships of the distal end of PZ with SCJ and PCA; A: all three at the same level, B: SCJ proximal to the other two which are at the same level, C: PCA distal to the other two which are at the same level, D: SCJ proximal to the distal end of PZ which is proximal to PCA. Cases with patterns B and D were thought to have E-BE, and those with patterns C and D to have E-HH. RESULTS: Patterns A, B, C and D were 79.2%, 12.1%, 3.8% and 4.9%, respectively. Length of PZ was 3.0 +/- 0.1 cm. E-BE and E-HH were found in 17.0% and 8.7%, respectively. Both E-BE and E-HH were more frequently found in males and in cases with reflux esophagitis. CONCLUSION: E-BE and E-HH are not so infrequent in Koreans as previously thought, if we use the distal end of PZ as an endoscopic marker of GEJ.
BACKGROUND/AIMS: Hepatic glucuronidating activity, essential for efficient biliary excretion of bilirubin, is reduced to about 30 percent of normal in patients with Gilbert's syndrome. Patients with Gilbert's syndrome have an additional TA insertion in the A(TA)TAA of UDP-glucuronosyltransferase 1 (UGT-1A1) promoter gene. This results in reduced frequency and accuracy of transcription initiation and enzyme activity. The frequency and location of the mutation vary according to races. This study was done to determine the UGT-1A1 promoter gene mutation in Korean cases of Gilbert's syndrome. METHODS: Promoter regions of the gene for bilirubin UGT-1A1 in twelve patients with Gilbert's syndrome and twenty healthy subjects (controls) were sequenced. RESULTS: 1) Among twelve Gilbert's syndrome five patients were homozygous for A(TA)6/6TAA, two were homozygous for A(TA)7/7TAA, and the other five were heterozygous for A(TA)6/7TAA. The prevalence of A(TA)TAA mutation was 58.3 percent. 2) Among twenty healthy subjects seventeen were homozygous for A(TA)6/6TAA, one was homozygous for A(TA)7/7TAA, and two were heterozygous for A(TA)6/7TAA. The prevalence of A(TA)TAA mutation was 15 percent. 3) The prevalence of A(TA)TAA mutation in Gilbert's syndrome patients was significantly higher than in the controls (p=0.018). CONCLUSION: Although the prevalence of A(TA)TAA mutation in Korean patients with Gilbert's syndrome is significantly higher than in the controls, the mutations of the promoter region of UGT-1A1 gene appear not to be the main or sole cause in Gilbert's syndrome in Korea since the prevalence of A(TA)TAA mutation is not so high. Further studies to determine the relationship between other UGT-1A1 gene mutation and Gilbert's syndrome in Korea are needed.
BACKGROUND/AIMS: Long-term lamivudine therapy can induce the emergence of lamivudine resistant hepatitis B virus (HBV) mutants. Clinically emergence of the mutant is expressed by the reappearance of disappeared HBV DNA in serum. Continued lamivudine treatment has been usually recommended in cases of viral breakthrough. However, the clinical outcome in patients with viral breakthrough is not clear. The aim of this study was to investigate the clinical course of chronic hepatitis B patients after viral breakthrough during lamivudine therapy. METHODS: A total of 74 patients with chronic hepatitis B who showed viral breakthrough after at least 6 months of lamivudine treatment were included in this study. They had positive HBeAg and HBV DNA before treatment. The median follow-up duration after breakthrough was 13 months. RESULTS: After viral breakthrough, only 8 patients (11%) maintained normal ALT levels and 66 patients (89%) showed elevation of ALT. 30 patients (41%) showed acute exacerbation of hepatitis (ALT increase over five-times upper normal limit). These acute exacerbations occurred within three months after breakthrough in 19 patients (63%). In the cases of acute exacerbation, 6 patients showed decompensated progression such as elevation of serum total bilirubin. One of them died of hepatic failure. A predictive factor for acute exacerbation was not found. HBeAg seroconversion occurred in 8 patients after viral breakthrough but their clinical course was highly variable. CONCLUSIONS: Chronic hepatitis B patients who had viral breakthrough during lamivudine therapy should be followed carefully and regularly in mind of potential clinical deterioration. New strategies are needed to manage the cases of acute exacerbation after viral breakthrough.